Ameliorative Effect Of Selenium Research Articles

Ameliorative effects of selenium against cypermethrin induced toxicity of tissue minerals in vital organs of Sprague Dawley rats

Publication history: Received on 26 October 2022; revised on 13 December 2022; accepted on 15 December 2022 Abstract: Introduction: Alpha-cypermethrin (Pyrethroid insecticide) is widely used in disease vector control, agriculture, home pest control and protection of foodstuff across the world. Due to its unchecked and widespread use, non-target organisms are also getting affected by its toxic effects. Objectives: This investigation was aimed to determine the preventive potential of selenium on changes in tissue minerals induced by a short-term (21 days) oral treatment of cypermethrin in Sprague-Dawley rats. Methodology: Female rats (n=20) were equally divided into four groups. Group 1 received corn oil (1 ml), Group 2 was administered 55 mg/kg/bw of cypermethrin, 1 ppm of sodium selenite was administered to Group 3 and Group 4 was given both cypermethrin and sodium selenite. Concentration of tissue minerals (Se, Na, K, Mg, Cu and Zn) were determined in the brain, heart, liver, kidney, spleen and blood through atomic absorption spectrophotometry. Results: Results showed that cypermethrin administration caused significant changes in trace metals and electrolytes in some of the tissues while most tissues’ concentrations remained unaffected. Conclusion: The present study showed that selenium can be effective in the protection of cypermethrin induced toxicity. However further studies can be conducted to analyze the effects of different doses of selenium on cypermethrin induced toxicity in tissue minerals.

Ameliorative effects of selenium against cypermethrin induced toxicity of tissue minerals in vital organs of Sprague Dawley rats

Ameliorative effects of selenium against cypermethrin induced toxicity of tissue minerals in vital organs of Sprague Dawley rats

Nickel Toxicity with Reference to Female Reproductive Physiology, Pregnancy and Teratogenesis: A Brief Review

Nickel has been known to adversely affect the female reproductive system and pregnancy, and cause teratogenesis. This review aims to analyse these effects of nickel. The implications of maternal oxidative stress and hormonal perturbations caused due nickel exposure have been discussed. Increased placental permeability, unidirectional foetal exposure through blood and milk leading to defects during organogenesis are analysed, along with post parturition eventualities such as stillbirth and altered sex ratios. Efforts are made to understand the ameliorative effects of selenium and possible future directions of research in the broad area are enumerated.

Selenium supplementation ameliorated paraquat-induced haemotoxicity in male rats

Introduction: The study was aimed at determining the haematological changes induced by 7 days paraquat exposure in rats and the ameliorative effect of selenium. Methods: Fifty-two adult male rats weighing between 150g and 200g were used for the study. The animals re randomly divided into five (5) groups of eight (8) rats each viz: Group I (DW) was administered distilled water only (2 ml/kg), group II (P1) was paraquat 15 mg/kg, group III (P1 + S) was paraquat (15 mg/kg) and selenium (0.3 mg/kg) an hour later, group IV (P2) was paraquat 30 mg/kg, while group V (P2 + S) was paraquat (30 mg/kg) and selenium (0.3 mg/kg) an hour later. Treatments were administered per os by gavage once daily for a week. Blood samples were analysed on the last day of administration. Results: The results of the study revealed that there were no significant differences (p >0.05) in haematological parameters in paraquat-induced toxicity in rats. Significance: The result of this research has shown that 7 days paraquat administration at 15 and 30 mg/kg has no detrimental effect on haematological parameters in rats, thus selenium supplementation cannot be justified to ameliorate its effect.

Selenium ameliorates cadmium-induced mouse leydig TM3 cell apoptosis via inhibiting the ROS/JNK /c-jun signaling pathway.

Despite the well-known acknowledgement of both the toxicity of cadmium (Cd) and the ameliorative effect of selenium (Se), the mechanism of the protective effect of selenium on cadmium-induced Mouse Leydig (TM3) cell apoptosis remains unknown. In this study, we hypothesized that the reactive oxygen species (ROS)-mediated c-jun N-terminal kinase (JNK) signaling pathway is involved in anti-apoptosis of selenium against cadmium in TM3 cells. We found that exposure to cadmium caused evident cytotoxicity, in which cell viability was inhibited, followed by inducement of apoptosis. Moreover, the level of ROS generation was elevated, leading to the phosphorylation of JNK. In addition, following cadmium exposure, the nuclear transcription factor c-jun was significantly activated, which led to increased expression of downstream gene c-jun, resulting in downstream activation of the apoptosis-related protein Caspase3 and upregulation of Cleaved-PARP, as well as inhibition of the anti-apoptosis protein Bcl-2. However, pretreatment with selenium remarkably suppressed cadmium-induced TM3 cell apoptosis. Furthermore, the level of ROS declined, and the JNK signaling pathway was blocked. Following this, the gene expression of c-jun decreased while Bcl-2 increased, which was consistent with the effects on proteins, that Caspase3 activity and Cleaved-PARP were inhibited while Bcl-2 level was restored. In order to explain the relationship between molecules of the signaling pathway, N-acetyl-L-cysteine (NAC), the ROS inhibitor, and JNK1/2 siRNA were administered, which further indicated the mediatory role of the ROS/JNK/c-jun signaling pathway in regulating anti-apoptosis of selenium against cadmium-induced TM3 cell apoptosis.

Sublethal Toxicity of Thiamethoxam Insecticide in Albino Mice: Biochemical, Oxidative Damage and Histopathological Evaluations

The Neonicotinoid insecticides are presently used in great amounts, but this can be a problem when the possible risks of occupational and environmental contamination are considered. The objective of this study was to investigate the potential adverse effects of sublethal doses of Thiamethoxam insecticide on serum biochemical, oxidative stress and histological alterations in male albino mice via 28-day repeated-dose oral toxicity study. The possible ameliorative effect of selenium plus vitamin E against the harmful effects of Thiamethoxam was also investigated. Mice in Thiamethoxam-treated groups received three sublethal doses (6, 12, and 30 mg/kg b.w./day). Animals in another group were orally co-administered selenium + vitamin E with the higher dose of insecticide. The results showed that Thiamethoxam significantly (p < 0.05) increased cholesterol levels and liver enzyme activities, in dose-dependent manner, compared to those of the control group. Levels of creatinine were not significantly changed, whereas uric acid increased at high doses. The oxidative stress parameters were significantly increased in association with decrease in total antioxidants level. The histological analysis revealed that the higher dose induced various alterations in tissues of vital organs, i.e. liver, kidney, lung and testes. Interestingly, the ameliorative effect of selenium + vitamin E in restoring the oxidative stress parameters was reflected by reducing severity of histopathological lesions. In conclusion, it appears that the sublethal dose < 6.0 mg/kg b.w./day, in repeated dose 28-day oral toxicity study, in male albino mice may be considered as No-Observed-Adverse-Effect-Level (NOAEL) of Thiamethoxam. Additionally, the antioxidant selenium, in mixture with vitamin E, showed an ameliorative effect against Thiamethoxam-induced toxicity.

Oxidative stress, hematological and biochemical alterations induced by sub-acute exposure to fipronil (COACH®) in albino mice and ameliorative effect of selenium plus vitamin E.

Fipronil (FIP) is a highly effective, broad-use insecticide that belongs to the phenylpyrazole chemical group. It is extensively used in the agriculture and veterinary medicine for controlling a wide variety of pests. Though FIP showed lower toxicity in vertebrates than in insects, it was recognized to have a variety of toxic effects in mammals. The present study was undertaken to evaluate FIP-induced alterations in the blood biochemical markers and oxidative stress parameters in male albino mice via oral sub-acute toxicity exposure. The possible ameliorative effect of the pretreatment with selenium plus α-tocopherol (vitamin E) against the harmful effects of FIP was also investigated. Mice in FIP-test groups were exposed to different sublethal doses, i.e., 1.43, 2.87, and 4.78 mg active ingredient (AI)/kg body weight (b.w.), equal to 1/100, 1/50, and 1/30 LD50 of FIP, respectively, for 28 days. Mice in the amelioration groups were orally administered with selenium + vitamin E (0.3 mg + 22.5 mg/kg b.w., respectively) 14 days prior to exposure to the higher dose (4.78 mg/kg) of FIP for another 14 days. Fipronil exposure at medium and high doses showed lowered values of red blood cell count (RBC), hematocrit (HCT), hemoglobin (HGB), white blood cell (WBC), and platelet (PLT) counts after 28-day exposure, compared to the control. All three doses caused significant increases in levels of liver-function biomarkers, i.e., aspartate amino transaminase (AST), alanine amino transaminase (ALT), alkaline phosphatase (ALP), cholesterol, and bilirubin levels compared to the control. Levels of biomarkers related to kidney functions, i.e., urea, uric acid, and creatinine, increased significantly than these of the control. Likewise, the oxidative stress indices, i.e., hydrogen peroxide (H2O2) and malondialdehyde (MDA), significantly increased at the higher and medium doses, while antioxidant enzymes, catalase (CAT) and superoxide dismutase (SOD), decreased significantly. On the other hand, prior administration of selenium + vitamin E in the FIP-exposed mice led to restore values of most hematological parameters nearly to these of the control. Also, the levels of AST, total protein, and creatinine seemed to be restored to the control values. Interestingly, pretreatment with selenium + vitamin E restored the levels of antioxidant enzymes, CAT and SOD, to the control values, whereas, oxidative stress indices, H2O2 and MDA, remained significantly high. It is our thought that the sublethal dose less than 1.43 mg/kg b.w. of commercial formulation of FIP (COACH® 200 SC) could be considered as no-observed-adverse-effect-level(NOAEL) under our present experimental conditions at short-term toxicity study. On the other hand, the higher sublethal doses, 4.78 and 2.87 mg/kg b.w., induced significant adverse effects in biomarkers and may be deleterious to human health following long-term exposure.

Clinicopathological Studies on the Ameliorative Effects of Selenium and Vitamin E against Cadmium Toxicity in Chickens

Cadmium (Cd) is one of the most dangerous environmental bioaccumulative heavy metals that concern a vital interest due to its injurious to animal and public health. An experimental trial was conducted for six weeks to evaluate the protective effect of selenium and /or vitamin E against the adverse effect of cadmium. One hundred and five, one day old broiler chicks were divided into five random groups. Group1 (negative control) was fed on basal diet; Group 2 was supplemented with 100 mg of cadmium /kg diet; Group 3 was supplied with 0.5 mg/kg diet of selenium; Group 4 was fed on 100 mg/kg diet of vitamin E and Group 5 was supplemented with Cd, Se and vitamin E combinations. The results revealed that cadmium group showed a highly significant increase in serum alanine amino transferase (ALT) and aspartate amino transferase (AST) (36±1.1and 220±3.53, respectively) activities, serum uric acid and creatinine (25.68±1.01 and 4.38±0.15, respectively) and a significant decrease in serum total proteins, albumin and globulins values (2.34±0.09, 1.14±0.05 and1.20±0.05, respectively) particularly at the end of the sixth week in comparable to the control group. In addition, a significant increase in serum malondialdehyde (MDA) and nitric oxide (NO) (3.9±0.09 and 51.33±0.88, respectively), a significant decrease in glutathione peroxidase (GSH-PX) values (0.05±0.005) associated with a significant reduction in interleukin 2 (IL2) and interleukin 10 (IL10) (1.8±0.30 and 7.4±0.43, respectively) values were reported specially at the end of the sixth week compared with the control group. Overall, our results showed an improvement in groups supplied with either Se or vitamin E when compared with cadmium group. In conclusion, supplementation of selenium or vitamin E alone didn’t recover the depressive effect of Cd but their combination could improve its deleterious effect due to their antioxidant activity.

BIOCHEMICAL AND PHYSIOLOGICAL ALTERATIONS INDUCED BY EXPOSURE TO THE INSECTICIDE FIPRONIL IN ALBINO MOUSE (MUS MUSCULUS).

The result of the present study indicate that exposure of fipronil, even at low doses and for a short-term period, can induce serious hepatic, renal and hematological damage, caused presumably by increased oxidative stress involves alterations indecreasing of antioxidant-enzymes, catalase (CAT) and super dismutase (SOD). Moreover, the Ability of fipronil to induce genotoxic effects involving structural chromosome aberrations (SCAs) and sperm-shape abnormalities. The mechanism of this genotoxic effects could be also attributed to reactive oxygen species (ROS)-mediated oxidative stress as pre-treatment with a known antioxidant, that is, vitamin E plus selenium has shown protective effect. In addition, pre-treatment with aqueous extract of ginger rhizomes (Zingiber officinale) showed beneficial effects in ameliorating the adverse effects of fipronil. Based on the overall findings from the present investigation, the estimated no-observed-adverse-effects-level (NOAEL) of fipronil formulation via sub-acute toxicity study could be less than 1.44 mg/kg b.w., equal to 1/100 LD50. The most important findings of this study are: ❖ Find out whether the selected sublethal doses of fipronil (FIP) formulation (COACH® 200 SC), administered orally to male albino mice, for 28 days, can cause any alterations in hematological and biochemical parameters. ❖ Determine the possible effects of sub-acute repeated dose exposure of FIP on oxidative stress indices and enzymatic antioxidants. ❖ Examine the histopathological modulations which may be happened by fipronil exposure in some vital organs, i.e. liver, kidney, spleen and testes. ❖ Explore the possible protective or ameliorative effects of selenium plus vitamin E (α- tocopherol) and/or extract of ginger rhizome (Zingiber officinale) against FIP-induced toxicity were determined.

Ameliorative Effects of Selenium in ZnO NP-Induced Oxidative Stress and Hematological Alterations in Catla catla.

Various applications of zinc oxide nanoparticles (ZnO NPs) can increase pollution in aquatic environments. Consequently, pollution can cause toxicity in fish as indicated by oxidative stress, hematotoxicity, and changes in gill and liver histology. Selenium is known for its antioxidant potential in scavenging the free radicals generated during ZnO NP-induced oxidative stress. This study tested the ameliorative role of selenium against ZnO NP-induced toxicity in freshwater fish Catla catla. Four groups of replicated fish, representing control, selenium-treated, ZnO NP-treated, and ZnO NPs+selenium-treated, were used in this study. The ZnO NPs (40mgl-1) were given to fish in water whereas selenium (50μgkg-1) was given as sodium selenite in feed. After 28days of exposure, the fish specimens were processed to collect samples of blood, gills, and liver. The results demonstrated that the consumption of selenium containing feeds protected the C. catla from ZnO NP-induced toxicity and oxidative stress. The use of selenium containing feeds appeared to have reduced the contents of glutathione S-transferase (GST) and glutathione reduced (GSH), and increased the level of catalase (CAT) and superoxide dismutase (SOD). Furthermore, the consumption of selenium in feeds improved the hematological parameters in ZnO NP-treated fish. This study suggests that dietary selenium might be able to ameliorate ZnO NP-induced toxicity in fish.

Ameliorative effects of selenium on arsenic-induced cytotoxicity in PC12 cells via modulating autophagy/apoptosis

Arsenic is well known toxicant responsible for human diseases including cancers. On the other hand, selenium is an essential trace element with significant chemopreventive effects, anticancer potentials and antioxidant properties. Although previous studies have reported antagonism/synergism between arsenic and selenium in biological systems, the biomolecular mechanism/s is still inconclusive. Therefore, to elucidate the molecular phenomena in cellular level, we hypothesized that co-exposure of selenium with arsenic may have suppressive effects on arsenic-induced cytotoxicity. We found that selenium in co-exposure with arsenic increases cell viability, and suppresses oxidative stress induced by arsenic in PC12 cells. Consequently, DNA fragmentation due to arsenic exposure was also reduced by arsenic and selenium co-exposure. Furthermore, western blot analyses revealed that simultaneous exposure of both metals significantly inhibited autophagy which further suppressed apoptosis through positively regulation of key proteins; p-mTOR, p-Akt, p-Foxo1A, p62, and expression of ubiquitin, Bax, Bcl2, NFкB, and caspases 3 and 9, although those are negatively regulated by arsenic. In addition, reverse transcriptase PCR analysis confirmed the involvement of caspase cascade in cell death process induced by arsenic and subsequent inhibition by co-exposure of selenium with arsenic. The cellular accumulation study of arsenic in presence/absence of selenium via inductively coupled plasma mass spectrometry confirmed that selenium effectively retarded the uptake of arsenic in PC12 cells. Finally, these findings imply that selenium is capable to modulate arsenic-induced intrinsic apoptosis pathway via enhancement of mTOR/Akt autophagy signaling pathway through employing antioxidant potentials and through inhibiting the cellular accumulation of arsenic in PC12 cells.

Ameliorative Effects of Selenium on Cadmium-Induced Injury in the Chicken Ovary: Mechanisms of Oxidative Stress and Endoplasmic Reticulum Stress in Cadmium-Induced Apoptosis.

Despite the well-established toxicity of cadmium (Cd) to animals and the ameliorative effects of selenium (Se), some specific mechanisms in the chicken ovary are not yet clarified. To explore the mechanism by which the toxicity effect of Cd is induced and explore the effect of supranutritional Se on Cd toxicity in female bird reproduction, forty-eight 50-day-old Isa Brown female chickens were divided randomly into four groups. Group I (control group) was fed the basic diet containing 0.2mg/kg Se. Group II (Se-treated group) was fed the basic diet supplemented with sodium selenite (Na2SeO3), and the total Se content was 2mg/kg. Group III (Se + Cd-treated group) was fed the basic diet supplemented with Na2SeO3; the total Se content was 2mg/kg, and it was supplemented with 150mg/kg cadmium chloride (CdCl2). Group IV (Cd-treated group) was with the basic diet supplemented with 150mg/kg CdCl2. The Cd, estradiol (E2), and progestogen (P4) contents changed after subchronic Cd exposure in chicken ovarian tissue; subsequently, oxidative stress occurred and activated the endoplasmic reticulum (ER) pathway to induce apoptosis. Further, Se decreased the accumulation of Cd in ovarian tissue, increased the E2 and P4 contents, alleviated oxidative stress, and reduced apoptosis via the ER stress pathway. The present results demonstrated that Cd could induce apoptosis via the ER stress pathway in chicken ovarian tissue and that Se had a significant antagonistic effect. These results are potentially valuable for finding a strategy to prevent Cd poisoning.

Alleviation of lead-induced oxidative stress and immune damage by selenium in chicken bursa of Fabricius.

We investigated lead (Pb)-induced oxidative stress and immune damage in the chicken bursa of Fabricius (BF) and the ameliorative effect of selenium (Se). Seven-day-old male chickens were randomly divided into four groups and were provided standard diet and drinking water, Na2SeO3 added to the standard diet and drinking water, standard diet and (CH3COO)2Pb added to drinking water, and Na2SeO3 added to the standard diet and (CH3COO)2Pb added to drinking water for 30, 60, and 90days. The presence of Pb inhibited total antioxidant capacity (T-AOC), glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities; decreased glutathione (GSH) content; increased malondialdehyde (MDA) and hydrogen peroxide (H2O2) contents; inhibited interleukin (IL)-2 and interferon-γ (IFN-γ) messenger RNA (mRNA) expression; and increased IL-4, IL-6, IL-10, IL-12β, and IL-17 mRNA expression. The presence of Se relieved all of the above Pb-induced changes. There were close correlations among GSH, CAT, T-AOC, SOD, GPx, MDA, and H2O2 and among IL-2, IL-4, IL-6, IL-12β, IL-17, and IFN-γ. Our data showed that Pb caused oxidative stress and immune damage in the chicken BF. Se alleviated Pb-induced oxidative stress and immune damage in the chicken BF.

Ameliorative Effects of Dietary Selenium Against Cadmium Toxicity Is Related to Changes in Trace Elements in Chicken Kidneys.

The ameliorative effects of selenium (Se) against cadmium (Cd)-induced toxicity have been reported extensively. However, few studies have assessed the effects of multiple ions simultaneously on the variations of elements. In this study, the changes in Se, Cd, and 26 other element concentrations were investigated in chicken kidneys. One hundred and twenty-eight 31-week-old laying hens were fed a diet supplemented with either Se, Cd, or both Se and Cd for 90days. The ion content was analyzed by inductively coupled plasma mass spectrometry (ICP-MS). We found that the Se, Cd, and combined Se and Cd treatments significantly affected the trace elements in the chicken kidneys. The Cd supplement caused ion profile disorders, including reduced concentrations of V, Cr, Mn, Mo, As, Ba, Hg, Ti, and Pb and increased Si, Cu, Li, Cd, and Sb. The Se supplement reduced the contents of Co, Mo, and Pb and increased the contents of Cr, Fe, and Se. Moreover, Se also increased the concentrations of Cr, Mn, Zn, and Se and decreased those of Li and Pb, which in contrast were induced by Cd. Complex interactions between elements were analyzed, and both positive and negative correlations among these elements are presented. The present study indicated that Se can help against the negative effects of Cd and may be related to the homeostasis of the trace elements in chicken kidneys.

Ameliorative effect of selenium on tomato plants grown under salinity stress

ABSTRACTThe ability of selenium (Se) to counteract salt inhibitory effects in crop plants, especially in tomato, is still poorly documented. In order to examine the impact of Se addition on the growth, some biochemical parameters related to osmotic adjustment and antioxidant defense of salt-stressed tomato, a two-factorial experiment was conducted in a greenhouse. The plants were supplied with NaCl (0, 25, or 50 mM) and Se (0, 5, or 10 μM), individually or simultaneously. The results showed that salinity had a deleterious impact on plant biomass and physiological parameters studied. The application of Se alleviated this adverse effect by improving the integrity of cell membranes and by increasing leaf relative water content under stress conditions. Moreover, the application of 10 μM Se significantly increased the photosynthetic pigments concentration under salt stress. Salt stress also caused an inhibition of catalase activity, but its activity was restored in the presence of Se. The free radical scavenging activity significantly increased in plants subjected to 25 mM NaCl and supplied with 5 µM Se, compared to NaCl-alone treatment. Both physiological and biochemical results indicate that 10 µM Se treatment can increase plant performance under salt stress, especially under high NaCl concentration.Abbreviations: CAT: catalase; Chl: chlorophyll; DPPH: 2,2-diphenyl-1-picrylhydrazyl; DW: dry weight; FW: fresh weight; POD: peroxidase; REL: relative electrolyte leakage; RWC: relative water content; free radical scavenging activity (FRSA); TW: turgid weight

Ameliorative effect of selenium in cisplatin-induced testicular damage in rats

In this study, we investigated the protective effect of selenium (Se) on cisplatin (Cis) induced testicular damage using histopathological, immunohistochemical and biochemical approaches. Twenty-one male Wistar rats were equally divided into three groups of seven rats each: control (C), Cis, and Cis+Se. Cis and Cis+Se group rats received Cis at a dose of 12mg/kg b.w./day, intraperitoneally for 3 consecutive days. Cis+Se group rats received selenium via oral gavage 3mg/kg/day (twice-a day as 1.5mg/kg) until 11th consecutive days starting at 5 days before cisplatin injection. C group received only 0.9% NaCl intraperitoneally and orally at same time and at equal volume. After the treatment, the histopathological, immunohistochemical and biochemical examinations were performed. In seminiferous tubules of Cis treated rats were observed the most consistent findings characterized with vacuolization, desquamation, disorganization, and also was a considerable reduction in elongated spermatids, however the Cis+Se group exhibited improved histopathologic changes. In the immunohistochemical examinations, caspase-3 immunopositive cells displayed higher in the Cis group according to C and Cis+Se groups. Bcl-2 and NF-κB staining revealed a moderate number in the C group and significantly fewer in the Cis group compared to the Cis+Se groups. Additionally, MDA levels were also significantly increased in the Cis group in comparison to Control group, but pretreatment with selenium prevented elevation of MDA levels significantly in Cis+Se group rats. This study indicates that Cis-treatment induced testicular apoptosis and lipid peroxidation, and combined treatment with selenium prevented severity of the toxicity in rats.

Ameliorative Effects of Selenium on Cadmium-Induced Oxidative Stress and Endoplasmic Reticulum Stress in the Chicken Kidney.

The harmful influences of dietary cadmium (Cd) on the chicken kidney and the protective role of selenium (Se) against Cd-induced nephrotoxicity in the chicken are relatively unexplored subjects. The aim of this study was to investigate the ameliorative role of Se on the effects of Cd-induced oxidative stress, endoplasmic reticulum stress, and apoptosis in chicken kidneys. For this study, 100-day-old chickens received Se (as 10 mg Na2SeO3/kg dry weight of diet), Cd (as 150 mg CdCl2/kg dry weight of diet), or Cd + Se in their diets for 60 days. Then, the histopathological changes, Cd and Se contents, levels of oxidative stress, inducible nitric oxide synthase-nitric oxide (iNOS-NO) system activity, levels of endoplasmic reticulum (ER) stress, results of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay of apoptosis, and expression levels of Bcl-2 and caspase 3 in the kidney were examined. The results showed that Cd exposure caused histopathological and ultrastructural damage and apoptosis of the kidneys. Cd administration significantly increased the accumulation of Cd, the malondialdehyde (MDA) content, NO production, iNOS activity, iNOS expression levels, expression levels of ER stress-related genes (GRP78, GRP94, ATF4, ATF6, and IRE) and the pro-apoptosis gene caspase 3, and the rate of apoptosis. Cd administration markedly decreased the Se content, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, and anti-apoptosis gene Bcl-2 expression levels. Co-treatment with Se and Cd obviously reduced the accumulation of Cd, Cd-induced histopathological and ultrastructural changes, oxidative stress, iNOS-NO system activity, ER stress, caspase 3 expression levels, and the rate of apoptosis in the kidneys. These results suggested that Cd exposure caused renal injury and that Se ameliorated Cd-induced nephrotoxicity in chickens.

The ameliorative effect of selenium on Azolla caroliniana grown under UV-B stress

Exposure of Azolla plants to UV-B radiation for 6 h resulted in a decrease in biomass and relative growth rate (RGR), which coincided with an increase in doubling time (DT) as compared with the control. Also, the protein content decreased. On the other hand, hydrogen peroxyde (H2O2) and malondialdehyde (MDA) accumulated significantly in UV-treated Azolla plants. Conversely, the addition of selenium (Se) at 1 ppm resulted in a significant increase in biomass and protein content of untreated and UV-treated Azolla plants, and a significant reduction in both H2O2 and MDA. Moreover, the addition of Se to UV-treated and untreated Azolla plants resulted in a significant increase in total ascorbate and total glutathione (GSH) contents compared with the control and UV-stressed Azolla plants. Also, glutathione redox potential (GSH/TG) increased significantly in UV-treated Azolla plants in the presence of Se. There also was a significant increase (38%) in ascorbate peroxidase (APX) activity in UV-treated plants compared with the control. APX activity in the presence of Se did not change significantly compared with the control. Glutathione reductase (GR) activity increased significantly in UV-treated Azolla, while glutathione peroxidase (GSH-PX) activity did not. On the other hand, both GSH-PX and GR activity in untreated and UV-treated Azolla plants were significantly enhanced by the application of Se to the nutrient media at a concentration of 1 ppm. Therefore, we can conclude that Se protects Azolla plants from UV-B stress.

Evaluation of ameliorative potential of selenium on carbendazim induced oxidative stress in male goats

In the present investigation, ameliorative effect of selenium on carbendazim induced oral sub chronic toxicity in bucks was assessed by studying various indices of antioxidant defense system. Bucks were randomly divided into four groups of four animals each. Group I served as control, Group II was orally drenched carbendazim at the dose rate of 50mg/kg body weight for 90 consecutive days. Group III was orally administered selenium in the form of sodium selenite at the dose rate of 0.05mg/kg body weight for 90 consecutive days. Group IV was orally administered carbendazim along with selenium at the same dosages as Group II and III. Prolonged administration of carbendazim produced oxidative stress in goat bucks as evidenced by increase in lipid peroxidation and decline in total antioxidant capacity. The increase in the activity of antioxidant enzymes was not sufficient to prevent pesticide induced oxidative stress. Selenium supplementation provides some amelioration against this effect. Further study is needed to prove ameliorative potential of this antioxidant against carbendazim induced toxicity in goat bucks.

Cadmium-Induced Injury and the Ameliorative Effects of Selenium on Chicken Splenic Lymphocytes: Mechanisms of Oxidative Stress and Apoptosis

Cadmium (Cd) is an important environmental pollutant present in soil, water, air, and food. Selenium (Se) can antagonize some metal element toxicity including Cd. To investigate the cytotoxicity of Cd and the protective effects of Se on bird immunocytes in vitro, chicken splenic lymphocytes with CdCl2 (10(-6) mol/L), Na2SeO3 (10(-7) mol/L), and the mixture (10(-7) mol/L Na2SeO3 and 10(-6) mol/L CdCI2) were incubated for 12, 24, 36, and 48 h, respectively. A high level of malondialdehyde (MDA) and reactive oxygen species (ROS) productions were observed in Cd treatment group; the activities of catalase (CAT), glutathione peroxidise (GSH-Px), superoxide dismutase (SOD), and the mitochondrial inner transmembrane potential (ΔΨm) were significantly lower in Cd treatment group than those in controls (P < 0.05 or P < 0.01). In contrast, Se significantly improved the activities of antioxidant enzymes and reduced MDA and ROS levels compared to Cd treatment alone group, although not restored to the levels of control group. The population of apoptosis cells demonstrated that Cd induces the apoptosis of chicken splenic lymphocytes; in addition, increased mRNA level of Bak, p53, caspase-3, caspase-9, and cytochrome c (Cyt c) and decreased Bcl-2, Bcl-xl, and CaM were observed in Cd treatment group. Se ameliorated ΔΨm and [Ca(2+)]i for mitochondria function restoring, and Se was able to modulate the expression of relative genes. In conclusion, concurrent treatment with Se reduced the Cd-induced morphological changes and oxidative stress, ion disorder, and apoptosis, suggesting that the toxic effects of Cd on the chicken splenic lymphocytes were partly meliorated by Se.