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The productivity and sustainability of livestock production systems are heavily influenced by animal nutrition. To maintain homeostatic balance in the body of the animal at different phases of life, the percentage of organically active minerals in livestock feed must be optimized. Selenium (Se) is a crucial trace mineral that is required for the maintenance of many functions of the body. Se nanoparticles (SeNPs) attracted considerable interest from researchers for a variety of applications a decade ago, owing to their extraordinary properties. SeNPs offer significant advantages over larger-sized materials, by having a comparatively wider surface area, increased surface energy, and high volume. Despite its benefits, SeNP also has toxic effects, therefore safety concerns must be taken for a successful application. The toxicological effects of SeNPs in animals are characterized by weight loss, and increased mortality rate. A safe-by-strategy to certify animal, human and environmental safety will contribute to an early diagnosis of all risks associated with SeNPs. This review is aimed at describing the beneficial uses and potential toxicity of SeNPs in various animals. It will also serve as a summary of different levels of SeNPs which should be added in the feed of animals for better performance. Keywords: Nanoparticles, Organism, Selenium, Toxicity, Trace minerals Introduction based on its integration into the active center of 25 seleno- Recent years have witnessed a growing academic interest proteins (SeLPs)  . Organic forms of Se and specific in nanotechnology development agriculture . Inorganic salts have been studied for many years , but elemental nanoparticles (NPs) are fast becoming a prospective in- Se nanoparticles (SeNPs) have recently received a great strument in animal feed. They promise an improvement deal of attention as a potential source of this vital compo- of properties of traditional mineral elements, through their nent . Figure 1 below illustrates the biological procep- biologic efficiency , bioavailability, or antimicrobial ef- tivity and effects of SeNPs which have been fects . NPs are recognized as particles less than 100 nm experimentally observed. in diameter, prepared by synthetic or biological ways. Pre- A few studies have shown that SeNPs have a lower vious studies have observed that NPs can maintain excel- toxic potency than dissolved ionic Se species, which is a lent bioavailability and decreased toxicity compared to promising finding . The evidence suggests that Se inorganic and organic formulae of trace minerals . The from NPs becomes less bioavailable to some extent . most frequently discussed mineral compound is selenium Furthermore, the toxicity of SeNPs could be reduced (Se) due to its narrow relationship between toxicity and through green synthesis or modification. Numerous ex- necessity for organisms . The biological efficacy of Se is periments of SeNPs toxicity have been conducted in ani- mals, but proper knowledge about the toxicological effects of SeNPs is insufficient. This review is aimed to * Correspondence: email@example.com 2 evaluate the updated information regarding the toxico- Department of Animal Nutrition and Forage Production, Mendel University in Brno, Zemedelska 1, CZ-613 00 Brno, Czech Republic logical effects of SeNPs in animals. Full list of author information is available at the end of the article © The Author(s). 2022 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 2 of 13 Fig. 1 The representation of some important biological prospects and effects of SeNPs Toxicity by selenium intake breathing difficulty, hepatocellular necrosis, kidney fail- Se poisoning is a threat in geographical areas with a high ure, heart attacks, and other cardiac disorders. Some re- abundance of Se in the environment. Continuous intake search has shown Se intoxication can delay the growth of water or feed rich in Se can lead to its accumulation of animals . Younger animals are more sensitive to and selenosis in the body . Acute Se poisoning of Se poisoning and the chemical forms may lead to differ- grazing animals occurs as a result of the consumption of ences in toxicity . In addition to mammals, Se has a a large number of accumulator plants with a high con- wide range of harmful consequences in birds, and the centration of in a short period of time. For example, sel- onset of toxicity varies from several hours to days . eniferous plants include prince’s plume, astragalus and The toxic effects in avian species include mortality, de- woody asters . According to scientific evidence, all creased growth, histopathological abnormalities, and species of animals are vulnerable to Se toxicosis. Symp- changes in hepatic glutathione (GSH) metabolism . toms of Se poisoning in mammals vary widely and in- clude nail abnormalities and loss of hair and wool , General mechanism of se toxicity weakness, vomiting, diarrhea, tiredness, reduced cogni- It has been shown that Se toxicity greatly depends on its tive function, lethargy, immobility, fatigue, weight loss, form. Generally, organic Se compounds are known to be itchy skin and mucous membrane irritation . Indi- less hazardous to cells than selenite, when investigated viduals who have the condition may experience lateral both in vitro and in vivo . Se species metabolize by sclerosis as well as irritation in the pharynx and bron- several pathways into different chemical forms, or they chial tubes, and may be recognized by a garlic smell on are incorporated into selenoproteins. In addition, due to their breath and in their sweat . the chemical similarity of Se with Sulphur, Se can be in- On the biochemical level, Se toxicosis includes spleno- volved in the biochemical pathways of thiol compounds. megaly, anemia, liver damage, and elevated ratios of bili- Scientific evidence shows Se can spontaneously interact rubin respectively . During the first 24 h after acute with glutathione to form Se , glutathiolseleol (GS-Se), poisoning, Se concentrations in the kidneys and liver selenodiglutathione (GS-Se-SG), hydrogen selenide drop by 80% from peak levels, according to animal stud- (H Se)  and selenotrisulfides. Selenotrisulfides can ies . An examination of Se poisoning in domestic an- react with other thiols to produce superoxide and hydro- imals has shown that there was an increase in the rate of gen peroxide, both of which are toxic . In addition, conception and the fetal resorption in bovine, sheep, and Se exposure promotes redox imbalance and the produc- horses fed naturally organic Se-containing diets with tion of reactive oxygen species in eucaryotic cells . 25–50 mg Se/kg  . Poisoning can also occur in swine, fish, and other grain-consuming species raised on sele- Mechanism of se induced genotoxicity niferous soils or, more often, due to errors in feed for- The genotoxicity of Se has been studied extensively. This mulation . genotoxicity occurs when an excess of ROS is present in Acute Se toxicity could lead to brain disorders, cells and reacts with cellular components. This causes changes in mental status, gastrointestinal symptoms, base lesions as well as breakage of deoxyribose nucleic Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 3 of 13 acid (DNA) strands via its reaction with both deoxyri- redox-active proteins, have been associated with suscep- bose sugars and the nucleobases of DNA. In addition, tibility to Se cytotoxicity by limiting intracellular cystine ROS oxidizes DNA, and Se interferes with DNA repair levels, according to another research group . As Se and transcriptional regulation, posing a threat to the sta- can modulate cell signaling pathways through the use of bility of genetic information. Further, Se also interacts a thiol redox system, it causes cytotoxicity through the with some DNA repair proteins that contain functional production of ROS, as well as by affecting the expression zinc (Zn) finger motifs, which are associated with signal- of correlating genes and proteins . ing pathways, such as DNA repair peptides, and DNA protein-protein interaction factors. Se can also interact The toxic effects of SeNPs with metallothionein and cause the release of Zn, which Various animal species have different sensitivities to the can affect DNA-binding capacity as well as genome sta- effects of Se and SeNPs. The toxicity of nanoparticles bility . Several authors have proposed that Se causes has mainly been studied in aquaculture due to these spe- genotoxicity by communicating with thiol groups by cies’ sensitivity to water pollutants. The toxicity of these means. On the other hand, it was discovered that SeNPs in aquaculture has been well documented and the number of dicentric chromosomes is roughly 2 times reviewed in recent studies. According to a review article higher in Se-plus radiation exposure treatment com- by Abbas et al., it has been implied that the nanoforms pared to the control group . In addition, Se causes of Se are particularly toxic compared to inorganic Se genotoxicity by interfering with the ataxia-telangiectasia salts . This finding is alarming in that most of the mutated gene and protein 53 expressions in the body. It nanomaterials used, including SeNPs, accumulate in the have been shown that mice treated with methylselenic environment and can reach fish that subsequently bio- acid and methyl selenocysteine in ten days treatment accumulate SeNPs in large quantities. In contradiction, delaying in the disease’s progression by increasing apop- however, it has also been reported that the SeNPs can tosis and decreasing proliferation was observed . increase the productivity of aquatic animals and improve their health in controlled experiments . Similar to Mechanism of se induced cytotoxicity the effect in mammals, the toxicological effect in fish de- Many researchers have investigated the cytotoxicity of pends on the dose, the chemistry of the SeNPs, and the Se, which causes irreversible changes in cells through a exposure time. Regarding the toxicity of SeNPs, this sec- variety of mechanisms. It has been found when cells are tion reviews the literature on toxicological studies of exposed to Se, the production of ROS can increase. Also, SeNPs. The findings are summarized in Table 1.To Se induces the production of ROS as a result of the sel- 2− compare SeNPs effect on the mammalian organisms the enide (Se ) reaction with thiol groups . Excess ROS chemoprotective studies of SeNPs are included in the damages not only lipids and proteins but also mitochon- Table 2. It is apparent, the SeNPs effects on organism drial membrane potential. According to one study, ROS- are greater than inorganic Se forms. In addition, the im- induced oxidative stress results from the activation of pact of Se on the health status depends on individual the mitochondrial apoptotic pathway . It has long need to create antioxidant defence. Otherwise, an excess been known that ROS causes cytotoxicity by activating of Se leads to its toxicity. The toxicity of SeNPs has been c-Jun N-terminal kinases (JNK), a subgroup of mitogen- thought to be related to Se toxicity in general. At higher activated protein kinases that regulates a wide range of concentration, both Se and SeNPs have pro-oxidative cellular functions including cell proliferation, differenti- properties leading to ROS production . This effect ation, and apoptosis. ROS can stimulate the JNK- could be enhanced by the bioaccumulation effect in sev- mediated tumor necrosis factor . ROS can also act as eral tissues where the liver is most sensitive. signal transduction pathway modulators, which can im- This area for the toxicological evaluation of SeNPs pact a variety of biological processes such as cell growth, have mainly focused only on antioxidant system per- apoptosis, and cell adhesion, among others . It has formance, body weight, and bioaccumulation in the liver, been discovered that Se, a constituent of SelPs, seems to kidney and heart. There is a paucity of literature on the have a close relationship with redox potential, which can interaction of SeNPs with the immune system, gastro- cause cytotoxicity by altering thioredoxin reductase intestinal tract, immune system, or bioaccumulation in (TrxR). This altered TrxR, when combined with thiore- muscles and other indirect targets of Se. Due to a large doxin (Trx), forms a potent dithiol-disulphide oxidore- surface area and small size, SeNPs and many other types ductase system . In addition to binding to signaling of nanoparticles seem to be more reactive and show bet- molecules (including apoptosis signal-regulating kinase- ter biodistribution in organisms compared to other 1 and Trx interacting protein), the system can also regu- forms of Se. Some studies described below have exam- late cell growth by interacting with the cells’ growth and ined the molecular mechanism of toxicity induced by survival mechanisms. Glutaredoxin proteins, which are Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 4 of 13 Table 1 Summary of toxicologic studies of SeNPs in various mammalian species Compare Animal Size, Modification Dose Exposed Effects LD50 Ref study species nm time, d Mice 35 0.1 mg Se/kg 45 SeNPs-M showed↑ Se retention and the levels of 72 mg/kg  diet glutathione peroxidase, superoxide dismutase and catalase Mice 20 200 μg Se/kg 90 Under the safe dose (0.75–7.5 mg/kg), oral 20 mg/kg  BW/d administration of PTR-SeNPs dramatically inhib- ited the growth of cancer in a tumor-bearing nude mouse mode Mice 40–55 2 mg Se/kg 28 SeNPs, caused↓ bone marrow cell death and  BW/d prevented DNA damage, compared to other forms of selenium Mice 20 0.5, 5, and 14 Toxicity ↑ when inorganic Se was applied than  50 mg Se/kg after subacute application of Sel-Plex, nanoSe, or diet LactoMicroSe Mice 70–90 1 and 4 mg 28 Nano-selenium at low dose (1 mg/kg) exhibited 113.87 mg/kg  Se/kg antioxidant effects in the liver compared to the high dose (4 mg/kg) of SeNPs and sodium selenite (1 and 4 mg/kg) Mice 50 Chitosan 10.5 g Se/kg 45 Acute fetal test showed SeNPs-C/C was safer than 8.8 mg/kg  selenite, with a median lethal dose (LD50) of ap- proximately 4-fold to 11-fold of that of selenite Na SeO Mice 5 2, 4 and 6 15 Selenite and SeNPs completely and partially 15.7 mg/kg  2 3 mg/kg BW suppressed mice growth respectively. Abnormal liver function was more pronounced with selenite treatment than SeNPs SeMetCys Mice 20–60 10 mg Se/kg 7 ↓Body growth, ireversible changes by SeMSC, SeMSC 14.6 mg  reversible changes by SeNPs in liver; ↑ serum ALT Se/kg and and LDH in SeMSC compared to SeNPs and ctrl. SeNPs 92.1 mg ↑ GST activity in SeNPs group compared to Se/kg SeMSC and ctrl; ↓ T-AOC in SeMSC group, not in SeNPs group SeMet Mice 20–60 10 mg Se/kg 7 ↑Gpx and thioredoxin reductase, ↓toxicity as 27.0 mg/kg  indicated by median lethal dose, acute liver injury, and short-term toxicity by SeNPs SeO Mice 80– Green 2.5, 5, 10, 20 14 ↓ Body weight, ↑ AST, ALT, ALP, Cr, Chol, TG, TB SeO2–7.3 mg/  220 synthetized via mg/kg BW and worsed hematological parameters in total kg SeNPs 198.1 Bacillus sp. blood at the dose of 20 mg/kg mg/kg Rats 78.88 2, 4, and 8 14 ↓ Antioxidant capacity in serum, liver, heart; ↓  mg Se/kg expression of GPx-1 and GPx-4 in liver; ↑MDA in BW liver Rats 79.88 0.2, 0.4, 0.8, 14 ↓ Body weight, ↑ ALP, SAST, CHol, ↑ liver weight;  2.0, 4.0,or ↓ thymus weight; ↑ Apoptotic cells count in liver 8.0 mg Se/kg BW Rats 4.6, κ-carrageenan- 500 μg/kg 10 ↓ Count of astroglial cells in brain; ↑ Se  24.5 capped SeNPs BW accumulation in liver, kidneys, brain in 4.6 nm SeNPs treated group; − changes in internal organs and glands Na SeO Rats 100– Green 5, 10, 15 μg/ 21 Organ weight in SeNPs groups; ↓ decreased  2 3 150 synthetized via kg weight of internal organs in sodium selenite potatoe extract, group; no differences in heamatological PEG coated parameters in sodium selenite group X markable changes in SeNPs group compared to ctrl; sodium selenite negatively affected; histopathology of liver, but not SeNPs; ↓ concentration of Se in breast milk in SeNPs compared to sodium selenite and ctrl group Na SeO Rats 20 0.05, 0.5,or 28 ↓ Body weight; − neurotransmitters,  2 3 4 mg Se/kg hematological parameters, histology of liver BW Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 5 of 13 Table 1 Summary of toxicologic studies of SeNPs in various mammalian species (Continued) Compare Animal Size, Modification Dose Exposed Effects LD50 Ref study species nm time, d Na SeO Rats 80 PVA modified 1.2 mg Se/kg 30 ↓ GSH in liver for Se, SeNPs groups; ↑ GSSG in liver  2 3 for Se, SeNPs groups; higher retention of Se in group of SeNPs compared to Se group in blood Rats 79.88 0.2, 0.4, 0.8 14 The supranutritional ↑ sperm motility and  mg Se/kg movement parameters, The nonlethal levels of BW 4.0 and 8.0 mg Se/kg BW ↓ testisweight, sperm concentration, and motility and also caused histopathological injury of testisand epididymis tissues to various degrees Rats 100 0.5, 1.5, 3.0 28 Histopathological examination showed damage 7 mg/kg  and 5.0 mg to the liver parenchyma and intestinal Se/kg epithelium, ↓ ALT activity Na SeO Rats 10, 18 mg/kg 10 CK, CK-MB and LDH levels of Group IV ↑ other 10 mg/kg  2 3 groups on both the 2nd and 10th days. In Groups II and III, this serum level decreased, and vitamin B ↑ Rats 5–100 2, 3, 4 and 5 91 The toxicity was ↑more pronounced in the 113 mg/kg  ppm selenite and high-selenium protein groups than the Nano-Se group Na SeO Rats 20–60 0.0096 and 14 SeNPs has a 7-fold lower acute toxicity than so- 15.7 mg/kg  2 3 0.1 ppm dium selenite in mice (LD50 113 and 15 mg Se/ kg body weight respectively Na SeO Rabbits 0.3 mg/kg 42 − Chol, TG, TP, Glu, ALT, AST, ↑ GPx mRNA 2 3 BW expression, TAOC Na SeO Chickens 100 Green 0.3 mg Se/kg 42 − Serum glucose, cholesterol, lipoprotein, thyroid  2 3 synthetized diet hormone, and liver function levels and biomarkers of kidney function; ↓ lowest relative weight of the liver; ↑ otal protein in serum Chickens 60 0.15, 0.30, 49 Se in serum, liver and breast muscle ↑, 113.0 mg/kg  0.60 and magnitude of increase was substantially ↑ when 1.20 mg/kg/d Nano Se was fed SeYeast, Chickens 0.1 and 0.3 42 SeNPs improved yellowness, redness and meat  SeMet mg/kg diet quality, NS and organic sources of Se resulted in better meat quality Chickens 100 0.3, 0.9 and 29 inorganic Se caused↓bioavailability in breast and  1.5 ppm duodenum tissue and↑ accumulation in organs involved in detoxification compared to organic selenium SeNPs Chickens 200 0.15, 0.30, 32 SeHME showed ↑ expression of GPx-4 in the  0.45 ppm livers and SelW in the spleens compared with SeS treatment Chickens 100 0.3, 0.9 and 29 Inorganic Se leads↓ bioavailability in breast and  1.5 ppm duodenum tissue and ↑ accumulation in organs involved in detoxification processes as compared to organic Se and SeNPs Sheeps 40 5 mg Se/kg 30 HB, RBCs, and PCV in Nano-Se ↓, SLD, GOT, CTT  BW and AP in Nano-Se group was↑. Levels of IgG, IgM, IgA, IL-2,TNF-α in NanoSe group were↓ than those of the control. SeMet, Piglets 28–59 0.3 mg Se/kg 28 ↑ Glutathion peroxidasis, expression of  Na SeO diet selenoprotein W (SELW), GPx1, and GPx3 in the 2 3 liver Pigs 100 0.5 mg Se/kg 45 − Performance; ↑ concentration Se in muscle, T-  diet AOC, GPx, SOD, CAT; ↓ MDA SeYeast Sheep 4 mg/kg 25 Ruminal pH, ammonia N concentration, molar  proportion of propionate, ratio of acetate to propionate ↓and total ruminal VFA concentration was ↑ with NS and YS Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 6 of 13 Table 1 Summary of toxicologic studies of SeNPs in various mammalian species (Continued) Compare Animal Size, Modification Dose Exposed Effects LD50 Ref study species nm time, d Na SeO Cows 100 0.3 mg Se/kg 30 −Matter intake, milk yield and composition; ↑  2 3 diet plasma Se levels and GPx; ↓ mRNA expression levels of glutathione peroxidase 1, 2 and 4; thioredoxin reductase 2 and 3; and selenoproteins W, T, K and F SeNPs, as well as the comparison of acute and long-term SeNPs with regard to GPx activity in plasma, liver and toxicity. kidneys. However, compared to Se-Met, SeNPs showed Most studies that have compared the toxicity of Se lower toxicity (LD 92.1 mg/Se/kg for Se-Met and 14.6 and SeNPs both agree well with the lower toxicity of mg/Se/kg for SeNPs) and fewer markers of acute liver SeNPs. Sublethal doses of 20 nm SeNPs at doses of 0.05, injury. A reduced accumulation of Se in dietary amounts 0.5, or 4 mg Se/kg body weight (BW)/d had no adverse and a higher lethal dose in mice fed SeNPs confirms the effect on brain neurotransimeters or hematological pa- possibility of using SeNPs to avoid Se toxicity . The rameters in rats compared to control and sodium proposed mechanism works via different absorption of selenite-treated groups group (0.5 mg Se/kg body Se by cells and their phase 2 response . weight/d) in a 28-day trial . In similar research, low While SeNPs have shown variable toxicological out- doses of SeNPs did not cause harmful effect during 48 comes, bionically or green synthesized and modified NPs days of treatment in rabbits. Both SeNPs and sodium have been reported which improving the effect on model selenite showed no significant changes in blood bio- animal health and reduce toxicity. The main advantage chemistry and liver enzyme activity at a dose of 0.3 mg/ of bionic NPs appears to be the mechanism of their syn- kg BW. Only liver PGx and T-AOC activity were in- thesis, which leads to the enrichment of SeNPs with bio- creased in Se-treated groups compared to the control active compounds. Because of this ability, bionic SeNPs group. Biochemical analysis was supported by higher have unique properties. The advantages of bionic and GPX-1 mRNA expression of 195% for Nano-Se and green synthesized NPs have been well-documented in 154% for sodium selenite . Higher doses of 2.0, 4.0 several review articles . To be specific for SeNPs, the and 8.0 mg Se/kg body weight of SeNPs administered for comparative study of Shakibaie et al.  was intro- 14 d caused increased body weight, increased liver en- duced. SeNPs (20,200 nm) were isolated from Bacillus zymes (ALT, AST) and cholesterol. Histopathological sp. and orally administered to rats at doses of 2.5, 5, 10 findings showed lesions in the liver, kidneys, lungs and and 20 mg Se/kg BW for 14 d. Compared to SeO , bionic thymus gland. The presence of apoptotic cells was also SeNPs showed a 26-fold lower LD , while no harmful observed, indicating that doses greater than 2 mg Se/kg effects on the organism were observed at a lower dose BW induced chronic toxicity . Similar findings were . Not only are bionic NPs able to reduce the toxic ef- found in male rats treated with SeNPs at doses of 2, 4 fect, but surface modifications make it possible to reduce and 8 mg Se/kg body weight for two weeks. Administra- the Se reactivity. κ-carrageenan-capped SeNPs (6.8 and tion of SeNP above 4.0 mg Se/kg body weight decreased 24.5 nm) at a dose of 2 mg/kg BW did not cause visible antioxidant capacities in the liver heart, and blood macroscopic or microscopic damage to major internal serum, and downregulated mRNA expression of GPX1 organs and systems in mice. However, an increased bio- and GPX4 in the liver. The proposed mechanism of accumulation of 6.8 nm SeNPs was found in liver, kidney SeNPs toxicity was further demonstrated in buffalo rat and brain. Further experiments within the same study liver cell lines. SeNPs at a concentration of 24 mol/L de- showed a size-dependent antioxidant activity of SeNPs, creased cell viability and damaged antioxidant capacity. while smaller SeNPs showed a higher ability to scavenge The decrease in cell viability induced by SeNPs was free radicals ABTS and DPPH. These results clarified mainly due to apoptosis but not cell necrosis . A that not only the size of SeNPs might play a role in Se comprehensive toxicological study showed that the 20– bioaccumulation, but their reactivity allows them to par- 60 nm SeNPs and Se-methionine in supranational ticipate in biochemical interactions with organic com- amounts (30 and 70 μg Se/kg BW) improved the Se ac- pounds . However, the vast majority of researchers cumulation in whole blood, liver and kidney in a dose- have not considered the long-term toxicity of SeNPs. To dependent manner compared to the control. At the diet- illustrate, in Xiao’s study, the first experiment showed an ary level of Se (1000 mg Se/kg BW), no improving effect enhancing effect of SeNPs (50 g Se/kg/d) in ApoE−/− of bioaccumulation in blood and tissues was observed in mice in an 8-week experiment . In another 24-week the case of SeNPs but not in Se-methionine form. No experiment, SeNP supplementation eliminated athero- difference was observed between Se-methionine and sclerotic lesions and increased antioxidant stress by Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 7 of 13 Table 2 Summary of original research articles focusing on the chemoprotective effect of SeNPs on various mammalian species Compare Animal Injury Size, Modification Dose Exposed Effects Ref. study species nm time, d Na SeO Mice Inducet atherosclerosis 23, 40, 50 μg 24 ↓ Atherosclerotic lesions; ↑ oxidative  2 3 86 Se/kg stress; ↓ GPx; ↑ hyperlipidemia in liver BW (observed changes were significantly higher in sodium selenite group; moreover SeNPs at the size of 40 nm showed highest negative impact on animal health) Na SeO Mice Alcohol-induced gastric 60 Chitosan 1.58–5 30 LD50 sodim selenite: 8.8 mg/kg BW; LD50  2 3 mucosal injury mg/kg SeNPs 73.2 mg/kg BW; − body weight, BW viscera indexes of heart, liver, spleen and kidney (not in liver); SeNPs showed gastroprotective properties; ↑ SOD, GSH- Px and CAT in gastric mucosa in SeNPs treated groups Mice Oxidative stress 50 Chitosan 10.5 60 Acute fetal test showed SeNPs-C/C was  mg/kg safer than selenite, with a median lethal dose (LD50) of approximately 4-fold to 11-fold of that of selenite Na SeO Mice 0, 2, and 8 Gy gamma 20–50 0.1 14 Selenium nanoparticles as an emerging  2 3 irradiation. mg/kg potent antioxidant agent can protect against irradiation induced nephropathy Mice oxidative stress 200 Melatonin 10 mg/ 10 MTse protects against hepatocellular  modified kg damage than a similar dose of melatonin SeNPs (10 mg/kg) or selenium (0.1 mg/kg) alone Mice Gentamyin induced 30–100 2 mg/ 10 SeNPs are potent antioxidant candidate  nephrptoxicity kg BW against GM-induced oxidative kidney tox- icity and hematoxicity in mice. Mice Eimeriosis-induced 5–50 0.5 5 SeNPs were able to regulate the gene  inflammation mg/kg expression of mucin 2, interleukin 1β, interleukin 6, interferon-γ, and tumor ne- crosis factor α in the jejunum of mice in- fected with E. papillata Mice Hepatocytes exposed to 50–200 0.10 14 Selenium nanoparticles bear a more  Gamma radiation mg/kg potent antioxidant effect in comparison with selenium selenite and can effectively protect the liver cell against Gamma radiation at a dose of 8.00 Gy Mice Cellular damage in thyriod by 3–20 0.5 5 Se nanoparticles have a protective effect  chromium mg/kg on K Cr O -induced thyroid damage, as a 2 2 7 result of correcting the free T and T 3 4 levels and GSH, catalase, SOD, and MDA compared to the K Cr O -treated group. 2 2 7 Rats Deltamethrin induced effects 100–200 0.5 60 ↑ Sperm count, motility and viability; ↑  on sperm characteristics mg/kg body weight; − testosterone; ↑ GPx, TAC; BW ↓ MDA Na SeO Rats Glycerol-induced acute 129.3 Green 0.5 14 ↑ Renal biochemical profile, GPx, ↓ MDA;  2 3 kidney injury synthesis mg/kg ↑ expression of IL-1β, IL-6, and TNF-α with genes; ↓ caspase-3, Bax, and cyt-c lycopene Rats Chloride-induced hepatorenal 100 0.4 21 − Creatinine levels; ↓ MDA; ↑ GSH, SOD in  toxicity mg/kg renal tissue; ↑ expression Bcl-2 (antiapop- BW totic protein); ↓ caspase-3 activity Na SeO Rats Paracetamole induced toxicity 40 0.5 and 30 − ALP, AST, ALT, LDH, GPx in Se and  2 3 1 mg/ SeNPs groups; protective effect of Se and kg SeNPs against paracetamol Rats Tert butyl hydroperoxid 42 0.3 35 ↓ SOD in liver in SeNPs and t-BHP treated  induced oxidative stress mg/kg rats compared to ctrl; ↑ GPx, CAT in liver BW in SeNPs groups; − liver enzymes among treated groups compared to ctrl Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 8 of 13 Table 2 Summary of original research articles focusing on the chemoprotective effect of SeNPs on various mammalian species (Continued) Compare Animal Injury Size, Modification Dose Exposed Effects Ref. study species nm time, d Rats Streptozocin induced 20–80 0.1, 0.2 28 ↓ Blood sugar, albumine in blood; ↓  diabetes and creatinin, urea 0.4 mg/kg BW Na SeO Rats Bisphenol-induced 20–60 2 and 70 ↑ Antioxidant status; ↓ MDA; ↑ restoration  2 3 reproductive toxicity 3 mg/ of testicular tissue; ↓ expression of mRNA kg BW of COX-2; ↑ expression of mRNA of ER-2; ↓ DNA fragmentation compared to ctrl and sodium selenite group Rats Induced bone toxicity 40–90 0.25, 28 ↑ Bone density and biochemical markers  0.5, 1 of bone resorption mg/ kg/d Rats Neurobehavioral Glycine 0.05 30 ↑ Rat’s behaviour and number of TH  abnormalities and oxidative and neurons; ↓ MDA; ↑ SOD and GSH-PX stress caused by 1-methyl-4- 0.1 phenyl-1,2,3,6- mg/kg tetrahydropyridine BW Rats Oxidative injury 50 Chitosan 280 30 ↑ Testicular function; ↑ testosterone levels,  mg/kg ameliorating testicular tissue; ↓markers of oxidative stress in male rats Rats Renal injury 68–122 0.1 14 ↑ Kidney relative weight; ↑ serum urea,  mg/kg creatinine, Kim-1, and renal malondialde- hyde, nitric oxide, TNF-α, IL-1β, cyto- chrome c, Bax, and caspase-3 levels Rats ACR-induced injury 25–51 Chitosan 0.2 60 Ch-SeNPs (0.2 mg/kg/d) displayed more  mg/ protection against ACR-induced damages kg/d comparing to Na SeO 2 3 Rats Reproductive toxicity 0.5 60 SeNPs improved DLM-induced negative  mg/kg effects on sperm characteristics, testoster- one, and antioxidant biomarkers, as well as behavioral and histopathological alter- ations. The SeNPs treated group showed improved semen parameters, antioxidant status, and sexual performance Rats Streptozotocin STZ-induced 10–80 0.1 28 SeNPs increased the glutathione content  diabetes mg/kg and antioxidant enzyme activities in testicular tissues. Moreover, microscopic analysis proved that SeNPs are able to prevent histological damage inthe testes of STZ-diabetic rats Rats Diabetic nephropathy during 2.5 42 SeNPs significantly reduced the rate of  pregnancy mg/kg urination, accelerated the start of gestation, and increased the percentage of successful pregnancy in females with DM Rats Carbon tetrachloride-induced 15–27 0.1 14 A high dose of SeNPsto rats with toxic  toxic damage of liver mg/kg liver damage decreases the concentration of lipid peroxidation products in the blood and normalizes the level of liver enzymes at a time of the damage of the urinary system Rats Carbon tetrachloride-induced 200–300 2.5 21 SeNPs pretreatment significantly improved  hepatotoxicity mg/kg the level of AST, urea, creatinine, MDA, LDH, and GSH in the CCl -injected rats towards the control levels Rats Cypermethrin-induced 100 2.5 21 SeNPs increased levels of GABA and  neurotoxicity mg/kg glutathione; on the other hand, it significantly prevented the rise in the Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 9 of 13 Table 2 Summary of original research articles focusing on the chemoprotective effect of SeNPs on various mammalian species (Continued) Compare Animal Injury Size, Modification Dose Exposed Effects Ref. study species nm time, d levels of MDA, TNF-α and IL-1β Rats Nephropathy 5 mg/ 30 Reduced glutathione and  kg malondialdehyde levels in tissue samples were correctly modulated in the pups from N.P.s treated diabetic mothers. Rats Cadmium chloride (CdCl )- 3–5, 0.5 56 SeNPs significantly ↓ CdCl -induced  2 2 induced neuro- and 10–20 mg/ elevation of serum kidney and brain nephrotoxicity kg damage biomarkers; lipid peroxidation; the percent of DNA fragmentation and nearly normalized the activity of acetylcholinesterase (AchE) and↑ activity and expression of antioxidant biomarkers Rats Brain oxidative damage 0.1 45 Enhanced brain antioxidant status and  mg/kg lower AChE activity and oxidative- inflammatory stress biomarkers. A signifi- cant downregulation of caspase 3 and upregulation of parvalbumin and Nrf2 protein expressions was observed in treated groups Rats MEL-induced renal function 3.3–17 Green 0.5 28 MEL-induced nephropathic alterations  impairments synthesis mg/kg represented by a significant increase in serum creatinine, urea, blood urea nitrogen (BUN), renal TNFα, oxidative stress-related indices Rabbits Thermal stress 50–400 Lactic 20 and 56 25 and 50 mg of nano-Se/kg diet,ncreas-  bacteria 50 mg/ ing the level of only BIO from a 25 to a assisted kg 50 mg/kg diet gave more improvement synthesis inthe studied parameter Chicken Heat stress 100–500 0.5 mL/ 38 Weight gain, performance index, behavioral  L indices, MDA,SOD,immunoglobulin G, immunoglobulin M, serum total protein, albumin, alanine aminotransferase, aspartate aminotransferase, and serum creatinine concentrations increased (P < 0.01) Chicken Oxidative stress by 100 Biogenic 0.6 42 Activity of cellular, humoral immune  enrofloxacin mg/kg response and enzymatic, non enzymatic antioxidants was significantly decreases as a result of EFX treatment Chicken Oxidative stress 10–45 0.3 42 Highest serum IgG and IgM  mg/kg concentrations were recorded for non- stressed birds received nano-selenium and organic selenium Chicken Cr((VI)) induced hepatic injury 0.5 35 Histopathological examination suggested  mg/kg that the liver cells of the Cr poisoning (VI) group were more severely injured than the nano-Se addition group. RT-qPCR re- sults showed that the relative expression of ACACA gene in the Cr poisoning (VI) group was significantly increased (P < 0.05), while the CPT1A gene’s expression was significantly decreased (P < 0.01) Na SeO Sows Induced heat stress (35 °C) 30–70 0.5 mg 25 ↓ Greatly mRNA level of Hsp70; ↑ mRNA  2 3 Se/kg level of Hsp27 diet Sows Induced heat stress (35 °C) 30–70 0.5 mg 25 ↑ Superoxide dismutase, catalase,  Se/kg superoxide dismutase, immunoglobulin G diet (IgG) and immunoglobulin A (IgA) in the serum and liver; ↓ malondialdehyde in the serum and liver Bano et al. Journal of Animal Science and Biotechnology (2022) 13:72 Page 10 of 13 inhibiting antioxidant enzymes. In addition, metabolic Declarations liver damage and hyperlipidemia have been observed. Ethics approval and consent to participate The negative effects were also size dependent, possibly Experiments on animals were not provided. due to cellular uptake. Nevertheless, the long-term tox- icity of SeNPs was still lower than that of sodium selen- Consent for publication ite . We consent to publication of the manuscript. In general, therefore, it appears that the toxicity of SeNPs is a function of several interrelated parameters Competing interests such as nanoparticle size and chemistry of the SeNP, We declare we do not have competing interests. dose, and exposure time that affect the biological re- Author details sponse of the organism. The results of toxicological Department of Physiology and Biochemistry, Faculty of Bioscience, Shaheed studies have shown that the main targets of the toxicity Benazir Bhutto University of Veterinary & Animal Sciences, Sakrand 67210, Pakistan. Department of Animal Nutrition and Forage Production, Mendel of SeNPs are not only prooxidative properties, but also University in Brno, Zemedelska 1, CZ-613 00 Brno, Czech Republic. Key their interactions with metabolic pathways and molecu- Laboratory of Veterinary Pharmaceutical Development, Ministry of lar signaling pathways, including apoptotic pathways, the Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences, Chinese Academy of Agricultural Sciences, Lanzhou 730050, China. ability of small nanoparticles to penetrate various tissues, and the organism’s ability to enzymatic transformation Received: 18 December 2021 Accepted: 14 April 2022 and eliminate Se. Conclusion References 1. Duhan JS, Kumar R, Kumar N, Kaur P, Nehra K, Duhan S. Nanotechnology: SeNPs and Se species have very similar mechanisms of the new perspective in precision agriculture. Biotechnol Rep. 2017;15:11–23. action and toxicity. The biggest differences in their ac- https://doi.org/10.1016/j.btre.2017.03.002. tion are due to their size and different reactivity. SeNPs 2. De M, Ghosh PS, Rotello VM. Applications of nanoparticles in biology. 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Journal of Animal Science and Biotechnology – Springer Journals
Published: Jun 17, 2022
Keywords: Nanoparticles; Organism; Selenium; Toxicity; Trace minerals
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