Effects of sarin on the operant behavior of guinea pigs

The present study evaluated the dose–response effects of subacute exposure to sublethal doses of the organophosphorus (OP) chemical warfare nerve agent (CWNA) sarin (GB) on the operant behavior of guinea pigs. Dietary restricted guinea pigs, trained to respond for food under a progressive ratio (PR) schedule of reinforcement, were injected five times per week (Monday–Friday) for 2 weeks with fractions (0.1, 0.2, and 0.4) of the established LD₅₀ of GB (42 μg/kg). Changes in body weight, whole blood (WB) acetylcholinesterase (AChE) levels, and operant performances were monitored over the 2 weeks of GB exposure and for an additional 2 weeks following the termination of exposures. There were dose-related changes in body weight and WB AChE levels throughout the exposure and post-exposure periods. Several parameters of PR performance were disrupted during exposure to 0.4 LD₅₀ GB, however, concurrent weight loss indicated the presence of overt toxicity. PR performance recovered following the termination of exposures. Lower doses (0.1 and 0.2 LD₅₀) of GB failed to produce reliable effects on operant performance during the exposure period. Overall responding decreased during exposure to 0.4 LD₅₀ GB, resulting in reduced response rates and break points. The decrease in overall response rates was attributed to an increase in pausing since there was no decrease in running rate. Motor effects of 0.4 LD₅₀ GB were evident as an increase in the proportion of lever press durations ≥ 1.0 s. In the present study, doses of GB lower than 0.4 LD₅₀ produced no marked alteration of operant performance in guinea pigs, although WB AChE levels were maximally inhibited to 20% of control.     

Effect of atropine on cyanide-induced acute lethality in mice

The effects of atropine on acute lethality induced by cyanide were investigated in mice. The LD₅₀ value of cyanide (s.c. injection) was 8.4 (7.6–9.3) mg/kg. However, the LD₅₀ value of cyanide (s.c.) was significantly increased by 1.5-fold when atropine (32 mg/kg) was injected s.c. in mice. Furthermore, the combined administration of atropine (32 mg/kg). Ca²⁺ (500 mg/kg) and sodium thiosulfate (1 g/kg) tremendously increased the LD₅₀ value by 5.6-fold in mice although sodium thiosulfate or Ca²⁺ alone increased the LD₅₀ 2.5- or 1.5-fold. On the other hand, although the LD₅₀ value of cyanide (intracerebroventricular injection (i.v.t.)) was 52.0 (47.4–57.0) μ/brain, the LD₅₀ value of cyanide (i.v.t.) was significantly increased by 1.3- or 1.61-fold in mice 10 min after s.c. injection of atropine (32 mg/kg) or Ca²⁺ (500 mg/kg). Furthermore, the combined administration of atropine and Ca²⁺ increased the LD₅₀ value of cyanide by 2.1-fold. These results suggest that atropine inhibits cyanide-induced acute lethality and promotes the antagonistic effect of thiosulfate and Ca²⁺ in mice.     

Activity and gene expression profile of certain antioxidant enzymes to microcystin-LR induced oxidative stress in mice

Microcystins are cyclic heptapeptide toxins produced by certain strains of Microcystis aeruginosa and microcystin-LR (MC-LR) is the most toxic among the 70 variants isolated so far. These toxins have been implicated in both human and livestock mortality. In the present study we investigated the microcystin-LR induced oxidative stress in mice in terms of its effect on activity and gene expression profile of certain antioxidant enzymes and expression of heat shock protein-70 (HSP-70). Mice were treated with 0.5 LD₅₀ (38.31 μg/kg) and 1 LD₅₀ (76.62 μg/kg) and the biochemical variables were determined at 1, 3, 7 days and 15, 30, 60 and 120 min post-exposure for 0.5 and 1 LD₅₀ dose, respectively. A significant time-dependent increase in HSP-70 expression over control was observed at 1 LD₅₀ dose. The toxin induced significant increase in liver body weight index, hepatic lipid perxoidation and depletion of GSH levels at 1 LD₅₀ compared to control group. There was significant decrease in the activity of antioxidant enzymes glutathione peroxidase (GPX), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione-S-transferase (GST) at 1 LD₅₀. Except catalase, there was no effect on other antioxidant enzymes at 0.5 LD₅₀ dose. In contrast to activity of antioxidant enzymes the gene expression profile did not show any significant difference compared to control at 1 LD₅₀. GR showed significant decrease in expression at 1, 3 and 7 days in animals dosed with 0.5 LD₅₀ MC-LR. The results of our in vivo study clearly show the oxidative stress induced by MC-LR, and a correlation with activity and regulation at gene expression level of antioxidant enzymes.     

Sodium arsenite inhibits migration of extravillous trophoblast cells in vitro

This study used a first-trimester human extravillous trophoblast (EVT) cell line, HTR-8/SVneo, to investigate whether sodium arsenite (AsNaO₂) reduces human EVT migration and invasion. Treatments with 2.5 μM AsNaO₂ or less (≤187.3 μg/L), concentrations that are relevant to human exposures in drinking water, were sublethal to HTR-8/SVneo cells. A 72-h exposure to sodium arsenite inhibited cell migration in a concentration-dependent manner at 0.625, 1.25 and 2.5 μM. Significant changes in cell proliferation were not observed under these treatment conditions. Moreover, inhibition of cell migration was unrelated to phosphorylation of focal adhesion kinase Tyr397. In contrast to cell migration, 72-h exposures to AsNaO₂ (0.3125–2.5 μM) had no significant effects on cell invasion, nor on the activities and protein expression of matrix metalloproteinase (MMP) 2 and MMP9. Because trophoblast migration is important for placentation, these results suggest an effect that could contribute to insufficiency of placental development and adverse pregnancy outcomes.     

Toxicity of the dialyzable fraction of the venom of the yellow scorpion, Leiurus quinquestriatus, to the migratory locust

Dialysis was carried out on redissolved freeze-dried venom of the scorpion Leiurus quinquestriatus H. and E. The mortality rate of Locusta migratoria migratorioides R. & F. injected with the dialyzable portion was used for calculating the regression equation and the LD₅₀. It was found that the LD₅₀ per female locust (mean weight 1·8 g) was that amount which was dialyzed out of 161 μg of whole venom, which means that the dialyzable portion has 2·67 per cent of the lethality of the whole venom. The toxic dose of the dialyzed venom was found not to differ from that of the whole venom.     

Genotoxicity analysis of the phenoxy herbicide dicamba in mammalian cells in vitro

The cytogenetic effects exerted by the phenoxy herbicide dicamba and one of its commercial formulations banvel^® (57.71% dicamba) were studied in in vitro whole blood human lymphocyte cultures. The genotoxicity of herbicides was measured by analysis of the frequency of sister chromatid exchanges (SCEs) and cell-cycle progression assays. Both dicamba and banvel^® activities were tested within 10.0–500.0 μg/ml doses range. Only concentrations of 200.0 μg/ml of dicamba and 500.0 μg/ml of banvel^® induced a significant increase in SCE frequency over control values. The highest dose of dicamba tested (500.0 μg/ml) resulted in cell culture cytotoxicity. The cell-cycle kinetics was affected by both test compounds since a significant delay in cell-cycle progression and a significant reduction of the proliferative rate index were observed after the treatment with 100.0 and 200.0 μg/ml of dicamba and 200.0 and 500.0 μg/ml of banvel^®. For both chemicals, a progressive dose-related inhibition of the mitotic activity of cultures was observed. Moreover, only the mitotic activity statistically differed from control values when doses of both chemicals higher than 100.0 μg/ml were employed. On the basis of our results, the herbicide dicamba is a DNA damage agent and should be considered as a potentially hazardous compound to humans.     

Immunotoxicity of paraquat after subacute exposure to mice

The immunotoxic effect of paraquat (PQ), a herbicide that has been used widely in agriculture was investigated using Balb/c mice. Paraquat was administered at doses of 1, 0.1, and 0.01 mg/kg for 21 days. Body weight, organ weight, cellularity of spleen, delayed type of hypersensitivity (DTH) response, plaque-forming cell (PFC) assay, hemagglutination titer (HA), quantitative hemolysis of SRBC (QHS) assay, spleen cell subtypes, cytokine production and lymphocyte proliferation assay were studied in various groups of animals. Results showed that high dose of PQ (1 mg/kg) could suppress both cellular and humoral activity of the immune system. PQ at medium dose (0.1 mg/kg) did not show any changes in organ weight, body weight and spleen cellularity but significantly decreased the proliferation response to PHA and the production of IFNγ. PQ at low dose (0.01 mg/kg) did not produce any significant changes in humoral or cellular responses of the immune system. In conclusion, paraquat at high dose has an inhibitory effect on the cell-mediated and humoral immunity. It seems that PQ has no adverse effects on mice immune system at low doses of 0.01 mg/kg, which is two times the PQ allowed daily intake (ADI) limit.     

Immunosuppression by chronic exposure to N-nitrosodimethylamine (NDMA) in mice.

Immunosuppression of humoral and cellular responses following chronic oral exposure to 1, 5, 10, and 20 ppm N-nitrosodimethylamine (NDMA) was examined in CD-1 mice. Monitoring of cumulative mortality and the incidence of peritoneal ascites in animals showed an NDMA dose-related mortality and hepatotoxicity. No visible changes in immunological parameters were noted at the 1 ppm NDMA dose. Immunosuppression of immunoglobulin M (IgM) antibody response by NDMA to sheep red blood cells (SRBC) was time-related, dose-related, and could be reversed within 30 d by removal of the chemical from the drinking water. Cellular immune response, monitored by allogeneic stimulation of cells in mixed lymphocyte reaction (MLR), was markedly suppressed by 10 and 20 ppm NDMA. Thus, chronic exposure to NDMA, except for the low-hepatotoxic doses of nitrosamine, resulted in a marked and persistent immunosuppression of cellular and humoral responses in CD-1 mice. In conclusion, chronic exposure to the hepatotoxic (ascite-inducing) doses of NDMA suppressed humoral and cellular immunity. The persistent immunosuppression could be reversed after the removal of NDMA from the drinking water. Although no direct NDMA-related cancer was reported in humans, our data point to a potential epigenetic carcinogenicity of nitrosamines due to chronic immunosuppression.     

The immune response of sheep to subclinical chronic exposure to the herbicide Bentazon TP.

A study of the effect of the Czechoslovakian herbicide BENTAZON TP on cells of the sheep immune system was carried out over a 3-mo period. A temporary decline in the number of T-lymphocytes in the peripheral blood was seen after 6 w of daily feeding of the herbicide. Dose-dependent statistically significant changes in the leucocyte migration index (p < 0.05) were seen at daily doses of 1/10 the LD50 (195 mg/kg body weight) and 1/20 the LD50 (97.5 mg/kg body weight) the 8th and 10th w of feeding, respectively. Significant changes of phagocytic activity and in the phagocytic index were not observed.     

Evaluation of the cytotoxicity of 10 chemicals in human and rat hepatocytes and in cell lines: Correlation between in vitro data and human lethal concentration

The cytotoxicity of 10 chemicals from the Multicentre Evaluation of In vitro Cytotoxicity (MEIC) list (nos 21–30) was evaluated in human and rat cultured hepatocytes and in two established cell lines (HepG2 and 3T3) according to the MEIC programme organized by the Scandinavian Society of Cell Toxicology. The MTT test was used as the endpoint of cytotoxicity after 24hr of exposure to the chemicals. Theophylline, phenobarbital and paraquat were the least cytotoxic compounds in the cellular systems (IC₅₀ = 450-17,000 μm) except for the 3T3 cells. The seven remaining chemicals (dextropropoxyphene, propranolol, arsenic trioxide, cupric sulfate, mercuric chloride, thioridazine and thallium sulfate) showed a similar relative cytotoxic ranking in the four in vitro systems in the lower range of concentrations (IC₅₀ = 2–350 μm). The data suggest that these 10 chemicals have a basal cytotoxic effect common to the four in vitro systems, and probably none of these compounds could be considered either hepatotoxic or species specific. The correlation between in vitro data and human lethal blood concentrations showed that the predictability of the in vitro systems was similar to that of in vivo rodent tests (LD₅₀) only when low cytotoxic concentrations (IC₁₀) were used for correlation.     

-Hydroperoxy diethyl peroxide, an unusual natural compound isolated from an ascidian (Phallusia mammillata): acute toxicity in DDY mice

-Hydroperoxy diethyl peroxide, a novel compound found in the tunic of ascidians, has two peroxide moieties per molecule. Since ascidians are a widely served food item in Japan, human exposure to this compound potentially exists in the seafood preparation industries. No toxicological data have so far been published on this compound, and so we determined the intraperitoneal 6-day LD₅₀ in mice and conducted histopathological examinations. The 6-day LD₅₀, was found to be 199 mg/kg with 95% confidence limits of 126–314 mg/kg. Histopathological examination revealed necrosis induced in a variety of cells that had been directly exposed to the compound. These cells included hepatocytes, parenchymal pancreatic cells and fat cells. It is concluded that direct contact with this compound is likely to elicit cellular necrosis of various organs. The specific toxicological effects are probably dependent on the route of exposure.     

An assay of the toxicity of the Atlantic puffer fish, Spheroides maculatus

Skin, muscle, liver, and gonadal extracts of the Atlantic puffer, Spheroides maculatus were assayed for toxicity in white mice. Extracts were injected intraperitoneally and were administered in the amounts of 1 ml per 20 g of body weight. The LD₅₀ of a composite skin extract, administered intraperitoneally in progressive doses per 20 g of body weight, was determined for white rats, white mice, chicks and frogs (Rana pipiens), while a LD₅₀ of a composite muscle extract was determined for the pinfish, Lagodon rhomboides.     

Human lymphocyte reactivity after in vitro exposure to technical and analytical grade pentachlorophenol

To investigate the potential effects of technical pentachlorophenol (PCP-T, contaminated with polychlorinated dioxins and furans) and of analytical grade pentachlorophenol (PCP-A) on the human immune system, in vitro assays with freshly prepared human peripheral blood lymphocytes were used as an alternative to experimental animals. Both cell-mediated and humoral immune functions were examined after direct lymphocyte exposure to PCP-T or PCP-A at concentrations ranging from 0–200 μM. In each case the viability of the treated cells remained within the control value range. T lymphocyte blastogenesis after 3 days incubation with PCP was measured using both optimal and suboptimal mitogen (PHA) concentration. Interleukin-2 activity of 24.5-h supernatants of lymphocytes in response to PHA, pretreated with PCP for 20–24 h, was examined in a bioassay using the mouse the IL-2-dependent CTLL-6 cell line. The synthesis of immunoglobulins was determined after stimulation with T-dependent (PWM) and T-independent (KlebsM) polyclonal B cell activators. In the proliferation assay the effects of PCP-T became more evident after suboptimal mitogen stimulation. Whereas after optimal mitogen stimulation blastogenesis was affected only at the highest concentration of 200 μM PCP-T, cell reactivity after suboptimal PHA stimulation was altered by all PCP-T doses. In the lower concentration range PCP-T caused enhanced proliferative responses, but at the two highest PCP-T concentrations cell reactivity was significantly suppressed as compared to the medium controls. Significant differences between the effects of PCP-T and PCP-A could be demonstrated only after optimal mitogen stimulation at the highest PCP concentration (200 μM). In contrast, lymphokine production as well as Ig secretion showed severe dose-dependent suppression after exposure to both PCP-T and PCP-A. The humoral immune response appeared to be more suppressed when cultures were stimulated with T-dependent rather than T-independent mitogens. The two different PCP preparations caused immunosuppression of both lymphocyte functions to the same extent. To summarize, the results of our studies indicate that PCP itself is directly immunotoxic to human immunocompetent cells and the T helper subset appears to be especially sensitive to PCP exposure. Furthermore, the observation of a direct effect on humoral immunity is similiar to previous results showing considerable alterations of antigen specific antibody production in experimental animals after in vivo exposure.     

The effects of zeta cypermethrin on the gills of common guppy Lebistes reticulatus

Effects of lethal and sublethal concentrations 15, 20, 26 and 35 μg/l of zeta cypermethrin on the gills of common guppies (L. reticulatus) were examined by light microscopy during 96 h exposure. The most common changes at all doses of zeta cypermethrin are the lifting of epithelial layer from gill lamellae and some necrosis. Besides the exudation, hyperplasia and the shortening of secondary lamellae were other histopathological effects. The 96 h LC₅₀ value for zeta cypermethrin to the L. reticulatus was determined 21.35 μg/l.     

Toxicokinetics and toxicity of thioacetamide sulfoxide: a metabolite of thioacetamide

Thioacetamide (TA) is bioactivated by CYP2E1 to TA sulfoxide (TASO), and to the highly reactive sulfdioxide (TASO₂), which initiates hepatic necrosis by covalent binding. Previously, we have established that TA exhibits saturation toxicokinetics over a 12-fold dose range, which explains the lack of dose–response for bioactivation-based liver injury. In vivo and in vitro studies indicated that the second step (TASO → TASO₂) of TA bioactivation is less efficient than the first one (TA → TASO). The objective of the present study was to specifically test the saturation of the second step of TA bioactivation by directly administering TASO, which obviates the contribution from first step, i.e. TA → TASO. Male SD rats were injected with low (50 mg/kg, ip), medium (100 mg/kg) and high (LD₇₀, 200 mg/kg) doses of TASO. Bioactivation-mediated liver injury that occurs in the initial time points (6 and 12 h), estimated by plasma ALT, AST and liver histopathology over a time course, was not dose-proportional. Escalation of liver injury thereafter was dose dependent: low dose injury subsided; medium dose injury escalated upto 36 h before declining; high dose injury escalated from 24 h leading to 70% mortality. TASO was quantified in plasma by HPLC at various time points after administration of the three doses. With increasing dose (i.e., from 50 to 200 mg/kg), area under the curve (AUC) and C_max increased more than dose proportionately, indicating that TASO bioactivation exhibits saturable kinetics. Toxicokinetics and initiation of liver injury of TASO are similar to that of TA, although TASO-initiated injury occurs at lower doses. These findings indicate that bioactivation of TASO to its reactive metabolite is saturable in the rat as suggested by previous studies with TA.     

The effect of sodium nitrite on some parameters of the immune system.

The effect of orally administered sublethal doses of 25, 50 and 100 mg/kg of sodium nitrite in drinking water ad lib. for 21 days on the immune response of Balb/c mice was investigated. The immunological parameters were examined at three phases: 1 day (phase A), 1 week (phase B) and 3 weeks (phase C) after the end of exposure to sodium nitrite. A significant decrease in dose-dependent manner was obtained in the following tests: lymphocyte percentages, concanavalin A (Con A)- and lipopolysaccharide (LPS)-induced lymphocyte proliferation assessed by the colorimetric MTT method, natural killer (NK) cell activity against WEHI-164 target cells, as well as IgM and IgG titers against injected sheep erythrocytes. Maximum suppressions were obtained in phase A after treatment with sodium nitrite at 100 mg/kg including lymphocyte count (17.5%), Con A-induced lymphocyte proliferation (40.1%), LPS-induced lymphocyte proliferation (31.4%), IL-2-stimulated NK cell activity (59.2%), unstimulated NK cell activity (59.6%), IgM titer (57.5%) and IgG titer (61.1%). On the other hand, a significant dose-dependent increase in neutrophil count (71.3%) in phase A and phagocytic activation (133%) in the first two phases was obtained using the nitroblue tetrazolium (NBT) assay in the presence of phorbol myristate acetate (PMA). It was found that the immunosuppressive effect of sodium nitrite is reversible after cessation of exposure.     

In vitro cytotoxicity tests for the prediction of acute toxicity in vivo

Investigations of the use of in vitro cytotoxicity tests for the prediction of acute toxicity in vivo have been reviewed with particular emphasis on those studies that have been published during the past 5 years. Numerous cell types, endpoints and exposure periods have been used in cytotoxicity tests, although these appear generally to have little effect on the resulting correlation between in vitro IC₅₀ values and in vivo LD₅₀ values. The in vitro data correlate better with rodent parenteral (ip or iv) LD₅₀ values than with oral LD₅₀ values due to kinetic considerations. For certain groups of related chemicals (e.g. antitumour compounds, metal salts), and for some sets of unrelated chemicals, the in vitro data correlate very well with LD₅₀ values. However, while cytotoxicity tests are useful for screening chemicals for their intrinsic and relative toxicities, it is impossible to tell whether predictions based on cytotoxicity data alone would be sufficiently accurate for labelling and classifying a new chemical according to its likely acute toxicity in vivo. The in vitro endpoints need to be of greater relevance to the possible mechanisms of chemically-induced acute toxicity in vivo than most of those that are used at present.     

Acute toxicity of inorganic selenium to Daphnia magna (Straus) and the effect of sub-acute exposure upon growth and reproduction

The acute toxicities of sodium selenite (Na₂SeO₃) and sodium selenate (Na₂SeO₄) to Daphnia magna were determined in defined culture at 22°C. For adults, the 48-h LC₅₀ values were 0.68 ppm selenium as selenite and 0.75 ppm selenium as selenate. Juveniles were more sensitive, with a 48-h LC₅₀ of 0.55 ppm selenium as selenate. Eggs and embryos were found to be much less sensitive, with a 72-h LC₅₀ of 1.4 ppm selenium as selenate.

Sub-acute exposure of D. magna to sodium selenate caused suppression of growth over instars 1–5 and reduced egg production in instar 9 when adults were exposed to test solutions from instar 6 onwards. These sublethal effects were found at concentrations in the range proposed as suitable for the use of selenium in the amelioration of mercury contamination.     

Effect of Acute Propanil Exposure on the Immune Response of C57BI/6 Mice

Effect of Acute Propanil Exposure on the Immune Response ofC57BI/6 Mice. BARNETT, J. B., AND GANDY, J. (1989). Fundam.Appl. Toxicol. 12, 757–764. Propanil is a herbicide thatis used extensively in rice farming to kill weeds without damagingthe rice plant The immunotoxic effects of acute exposure topropanil were determined in adult C57B1/6 female mice exposedintraperitoneally to propanil at doses of 0, 10, 25, 50, 100,200,or 400 mg/kg body wt. One week following exposure, the immunecompetency of the animals was assessed. Contact hypersensitivityresponse (CHR), blastogenic response to T- and B-cell-specificmitogens, and mixed lymphocyte reaction (MLR) were significantlydepressed only in propanil-treated animals at 400 mg/kg. However,the number of splenic antibody-producing cells was also significantlydepressed in a dose-dependent manner at the lower doses of 50,100, and 200 mg/kg. In addition, a significant reduction inthe thymus weight and an increase in absolute and relative spleenweight were also measured in animals treated with 200 and 400mg/kg. The increase in spleen weight also showed a concomitantrise in spleen cellularity. These data indicate that propanilhas a dose-dependent immunotoxic effect on the adult mouse thataffects primarily the humoral response     

Stannous chloride induces alterations in enzyme activities, lipid peroxidation and histopathology in male rabbit: Antioxidant role of vitamin C

Stannous chloride (SnCl₂) is widely used in daily human life to conserve soft drinks, in food manufacturing and biocidal preparations. It had genotoxicity, immunotoxicity, neurotoxicity and oxidative stress. Therefore, the present experiment was carried out to determine the effectiveness of l-ascorbic acid (AA) in alleviating the toxicity of SnCl₂ on some enzyme activities and oxidative damage in male New Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0 mg AA and 0 mg SnCl₂/kg BW (control); 40 mg AA/kg BW; 20 mg SnCl₂/kg BW (1/500 LD₅₀); 20 mg SnCl₂ plus 40 mg AA/kg BW. Rabbits were orally administered the respective doses every other day for 12 weeks. Liver and kidney specimens were processed for histopathologic studies. Results obtained showed that SnCl₂ significantly (P < 0.05) induced free radicals in rabbit liver, testes, kidney, lung, brain and heart. While, the activity of glutathione S-transferase (GST) and the level of sulfhydryl groups (SH-group) were decreased (P < 0.05) in all tested organs except brain and heart. Aspartate aminotransferase (AST) activity was increased (P < 0.05) in liver and decreased in testes, but alanine aminotransferase (ALT) did not change. The activities of alkaline phosphatase (AlP) and acid phosphatase (AcP) were decreased (P < 0.05) in liver, testes, kidney and lung. Also, the activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma of rabbits treated with SnCl₂ compared to control group. Histopathologic studies showed marked changes in hepatocytes as well as proliferation of duct epithelium, dilatation and congestion of blood vessels as well as mononuclear inflammatory infiltrate. The kidney were also severely affected by SnCl₂ the Bowman’s space was increased, with infiltration of renal parenchyma by mononuclear inflammatory infiltrate and changes in cells lining convoluted tubule. Ascorbic acid alone significantly decreased the levels of free radicals, and increased the activity of GST and the levels of SH groups in tested organs except brain and heart. While, the rest of the tested parameters were not affected. Results showed that AA alleviated the harmful effects of SnCl₂. This was proved histopathologically by the great improvement in liver and kidney histology where hepatocytes retained normal architecture with mild dilatation and congestion of blood vessels. Bowman’s space of kidney was almost normal, with normal lining of proximal and distal convoluted tubules. In conclusion AA could be effective in the protection against stannous chloride toxicity.