Testicular toxicity of orally administrated bisphenol A in rats and protective role of taurine and curcumin.

Bisphenol A (BPA) is an endocrine disrupting chemical widely used in the world. Curcumin, the yellow bioactive compound of turmeric has demonstrated its antioxidant activities. Taurine is a low-molecular weight organic compound in living organisms. The present study was aimed to investigate the adverse effects of BPA and its protection by taurine and curcumin. Oral BPA, curcumin and taurine administration in adult male rats at 130mg/kg bw, 100mg/kg bw and 100mg/kg bw, respectively for four weeks. Pathology and oxidative damages were investigated. The results show that BPA increased malondialdehyde (MDA) levels and decreased antioxidant enzyme activities [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST)] in testes of rats compared to the control group. Co-treatment with curcumin or taurine with BPA led to reduce in MDA and increased GPx, GST, CAT, SOD activities compared to BPA group. Furthermore, while some pathological findings were observed in testis tissues in BPA treated group, less histopathological findings were shown in BPA plus curcumin and/or taurine treated groups. Consequently, curcumin and taurine significantly protect BPA induced testicular damage in rats.

Mercuric chloride induced hepatotoxic and hematologic changes in rats: The protective effects of sodium selenite and vitamin E.

This study focuses on investigating the possible protective effect of sodium selenite (Na2SeO3) and/or vitamin E against mercuric chloride (HgCl2)-induced hepatotoxicity in rat. Male rats were given HgCl2 (1 mg/kg body weight (bw)) and HgCl2 plus Na2SeO3 (0.25 mg/kg bw) and/or vitamin E (100 mg/kg bw) daily via gavage for 4 weeks. HgCl2-treated groups had significantly higher white blood cell and thrombocyte counts than the control group. Serum activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl-transferase, and lactate dehydrogenase significantly increased and serum levels of total protein, albumin, triglyceride, total cholesterol, and low-density lipoprotein cholesterol significantly decreased in the HgCl2-treated groups compared with control group. Malondialdehyde level significantly increased and superoxide dismutase, catalase, and glutathione peroxidase activities decreased in liver tissue of HgCl2-treated rats. Also, HgCl2 exposure resulted in histopathological changes. Supplementation of Na2SeO3 and/or vitamin E provided partial protection in hematological and biochemical parameters that were altered by HgCl2 As a result, Na2SeO3 and/or vitamin E significantly reduced HgCl2-induced hepatotoxicity, but not protected completely.

In vitro effects of quercetin on oxidative stress mediated in human erythrocytes by benzoic acid and citric acid.

Benzoic acid (BA) and citric acid (CA) are food additives commonly used in many food products. Food additives play an important role in food supply but they can cause various harmful effects. The in vitro adverse effects of BA and CA and the protective effect of quercetin on human erythrocytes were investigated by measuring malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities. Erythrocytes were incubated with BA and CA, at three doses of 50, 100 and 200 microg/ml, and quercetin, at a concentration of 10 microM. After BA and CA application, a dose-dependent increase in MDA level and decreases in SOD, CAT, GST and GPx activities were found in erythrocytes. Among the two food additives, BA exerted a more harmful influence on human erythrocytes than CA. The protective effects of quercetin against oxidative stress--induction in the human erythrocytes by CA and BA, were found when these two food additives were applied at each of three doses of 50, 100 and 200 microg/ml. However, complete protection of quercetin against CA toxicity was only observed when this agent was applied at a lower dose of 50 microg/ml. Quercetin did not completely protect erythrocytes even at the lowest concentration of BA.

Investigating the impact of different routes of nano and micro nickel oxide administration on rat kidney architecture, apoptosis markers, oxidative stress, and histopathology.

Although the production and use of nickel oxide nanoparticles (NiONP) are widespread, environmental and public health problems are associated with it. The kidney is the primary organ in excretion and is among the target organs in nanoparticle toxicity. This study aimed to compare the renal toxicity of nickel oxide (NiO) microparticles and nickel oxide nanoparticles by different routes of administration, such as oral, intraperitoneal (IP), and intravenous (IV). Seven groups were formed, with 42 male rats and six animals in each group. NiO oral (150 mg/kg), NiO IP (20 mg/kg), NiO IV (1 mg/kg), NiONP oral (150 mg/kg), NiONP IP (20 mg/kg), and NiONP IV (1 mg/kg) was administered for 21 days. After NiO and NiONP administration, a decrease in antioxidant activities and an increase in lipid peroxidation occurred in the kidney tissue of rats. Increased kidney urea, uric acid, and creatinine levels were observed. Inhibition of acetylcholinesterase activity and an increase in interleukin 1 beta were detected. Apoptotic markers, Bax, caspase-3, and p53 up-regulation and Bcl-2 down-regulation were observed. In addition, histopathological changes occurred in the kidney tissue. In general, it was observed that nickel oxide microparticles and nickel oxide nanoparticles cause inflammation by causing oxidative stress in the kidney tissue, and NiONP IV administration is more effective in renal toxicity.

Comparison of nickel oxide nano and microparticles toxicity in rat liver: molecular, biochemical, and histopathological study.

The unique properties of nickel oxide nanoparticles distinguish it from classical nickel compounds, increasing its use in agriculture, industry, and many industrial areas. The aim of this study is to investigate the possible toxicity of nickel oxide and nickel oxide nanoparticles in the liver. For this purpose, Wistar rats were given nickel oxide and nickel oxide nanoparticles orally, intraperitoneally, and intravenously for 21 days. Liver organ weight, biochemical and hematological parameters, oxidative stress (malondialdehyde, catalase, superoxide dismutase, glutathione peroxidase, and glutathione S transferase), acetylcholinesterase activities, inflammation levels, apoptotic markers, and histopathological changes were evaluated comparatively. When the data obtained were examined in general, it was observed that nickel oxide nanoparticles caused more hepatotoxicity in liver tissue than nickel oxide in terms of oxidative stress parameters, apoptotic markers, inflammation indicators, and other parameters examined. The results suggest that toxicity induced by both nickel oxide and nickel oxide nanoparticles plays an important role in hepatocyte apoptosis.

Lead nitrate and cadmium chloride induced hepatotoxicity and nephrotoxicity: Protective effects of sesamol on biochemical indices and pathological changes.

Lead nitrate (LN) and cadmium chloride (CdCl2 ), regarded as environmental contaminants, are toxic heavy metals. Sesamol is a dietary phytochemical found in sesame oil. We aimed to analyze the hepatotoxic and nephrotoxic effects of LN and CdCl2 and to evaluate the possible protective effect of sesamol. LN (90 mg/kg bw per day), CdCl2 (3 mg/kg bw per day), and sesamol (50 mg/kg bw per day) were given to rats via gavage for 28 days. Total protein, albumin, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, total cholesterol, urea, uric acid, creatinine, superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, malondialdehyde, acetylcholinesterase, and histopathological changes were investigated in liver and kidney tissues. Lead and cadmium were found to result in decreases in the antioxidant enzymes and acetylcholinesterase activities, increases in malondialdehyde levels, and changes in serum biochemical parameters and various pathological findings. An improvement in all these parameters was observed in the sesamol-treated groups. PRACTICAL APPLICATIONS: Heavy metals are used in many areas of the industry all over the world. Heavy metals which include lead nitrate and cadmium chloride cause cell damage by oxidative stress. Some of the examining parameters for oxidative stress are SOD, GST, MDA, GPx, and CAT. However, some chemicals such as sesamol are well-liked and widely used as antioxidants against xenobiotic toxicity. We also indicate that sesamol has been shown to protective effect against heavy metals caused cell damage.

Malathion-induced oxidative stress in human erythrocytes and the protective effect of vitamins C and E in vitro.

Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in erythrocytes through the generation of free radicals and alteration of the cellular antioxidant defense system. We examined the effect of several different doses of malathion (25, 75, 200 microM), or malathion in combination with vitamin C (VC; 10 microM) or vitamin E (VE; 30 microM), on the levels of malondialdehyde (MDA), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in human erythrocytes in vitro. Erythrocytes were incubated under various treatment conditions (malathion alone, vitamins alone, or malathion plus vitamin) at 37 degrees C for 60 min, and the levels of MDA, and SOD, CAT and GPx activities, were determined. Treatment with malathion alone increased the levels of MDA and decreased SOD, CAT, and GPx activities in erythrocytes (P < 0.05). There were no statistical differences among VC-treated, VE-treated, or VC + VE-treated erythrocyes, as compared with nontreated control cells. Treatment of cells with malathion + VC, malathion + VE, or a combination of all three agents prevented malathion-induced changes in antioxidant enzyme activity and lipid peroxidation. However, this effect was seen only at low concentrations of malathion (25 and 75 microM), and the combination of VC + VE had a more protective effect than VC or VE alone. These results indicated that the presence of vitamins at concentrations that are similar to the levels found in plasma have no effect on malathion-induced toxicity in erythrocytes at a concentration of malathion (200 microM) that is typically used in pesticides.

Histopathological and biochemical studies on the effect of curcumin and taurine against bisphenol A toxicity in male rats.

Bisphenol A (BPA) is a chemical found in environmental xenoestrogen. In the present study, olive oil, curcumin, taurine, BPA, curcumin plus BPA, and taurine plus BPA were exposed to rats for 4 weeks via gavage. Content of malondialdehyde and activities of antioxidant enzymes (GPx, GST, SOD, CAT) and also histopathological and cytopathological changes of heart were studied. No significant changes in all studied parameters were seen between control, olive oil, curcumin, and taurine-treated groups. However, there were significant differences in levels of malondialdehyde and activities of antioxidant enzymes in BPA-exposed rats and some histo/cytopathological changes determined. In curcumin plus BPA-exposed and taurine plus BPA-exposed groups, we measured the preventive effects on some parameters but not exactly. As a result, curcumin and taurine significantly minimized BPA-induced cardiotoxicity in rats.

Bendiocarb induced histopathological and biochemical alterations in rat liver and preventive role of vitamins C and E.

In this study, biochemical changes and histological structure of rat liver after bendiocarb administration and possible preventive effects of vitamins C and E were studied. The animals were given with bendiocarb, vitamin C and vitamin E, daily 0,8mg/kg of body weight (bw), 100mg/kg-bw and 100mg/kg-bw for 28days, respectively. Lipid peroxidation, antioxidant enzyme activities, histological alterations and antioxidant capacity assays of liver and also liver function tests and lipid profile were measured. Bendiocarb treatment decreased the antioxidant enzyme activities, FRAP and TEAC values and increased malondialdehyde levels compared to control. Also, there were statistically significant alterations in liver function tests, lipid profile parameters and histopathological changes in bendiocarb treated groups. Vitamins C and E showed protective effects against examining parameters. According to results we can say that co-treatment of vitamin C and vitamin E may be more effective than use of them alone.

Effects of diazinon on pseudocholinesterase activity and haematological indices in rats: The protective role of Vitamin E.

Diazinon (DZN) is an organophosphate insecticide has been used in agriculture and domestic for several years. Vitamin E (200mg/kg, twice a week), diazinon (10mg/kg, per day) and Vitamin E (200mg/kg, twice a week)+diazinon (10mg/kg, per day) combination were given to rats orally via gavage for 7 weeks. Pseudocholinesterase in serum and haematological indices were investigated at the end of the 1st, 4th and 7th weeks comparatively with control group. At the end of 1st, 4th and 7th weeks, statistically significant decrease of pseudocholinesterase activity in serum were detected when diazinon- and Vitamin E+diazinon-treated groups compared to control group. When diazinon- and Vitamin E+diazinon-treated groups were compared to each other there were no significant changes. When diazinon-treated group was compared to control group, body weight decreased significantly at the end of the 4th and 7th weeks. It was observed that at the end of 1st, 4th and 7th weeks, there was a statistically significance in haematological indices except mean corpuscular hemoglobin (MCH) when diazinon-treated group was compared to control group. At the end of 1st week increase of thrombocyte, at the end of the 4th week increase of hemoglobin and thrombocyte and at the end of the 7th week increase of red blood cell (RBC), hemoglobin, hematocrit, mean corpuscular hemoglobin concentration (MCHC) and thrombocyte were observed statistically significant when Vitamin E+diazinon treated group was compared with diazinon treated group. According to the present study, we conclude that Vitamin E reduces diazinon toxicity, but it does not protect completely.

Furan-induced hepatotoxic and hematologic changes in diabetic rats: the protective role of lycopene.

Furan forms as a result of thermal treatment of food and induces harmful effects on organisms. In our work, lycopene, furan, and a combination of the two were given to diabetic male rats for 28 days. Hematological changes, total protein and cholesterol, triglyceride, and albumin levels, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase activities of the serum, malondialdehyde levels, glutathione peroxidase, catalase, glutathione-S-transferase, superoxide dismutase activities, DNA damage in liver tissues and hepatic histopathological alterations were compared to a control group. There were significant changes in the liver function tests, DNA damage, activities of antioxidant enzymes, and malondialdehyde levels between diabetic control and non-diabetic control groups, between diabetic control and diabetic lycopene groups, and also between diabetic furan and diabetic control groups. In diabetic lycopene and diabetic furan + lycopene treated groups we designated the preventive effects of lycopene against diabetes and furan, however, on the analysed parameters only. In spite of some pathological alterations designated in diabetic furan treated group's liver, fewer pathological alterations were observed in furan+lycopene treated groups at the end of week 4. Consequently, lycopene significantly reduced furan- and diabetes-induced toxicity in rat liver.

Subacute effects of low dose lead nitrate and mercury chloride exposure on kidney of rats.

Lead nitrate and mercury chloride are the most common heavy metal pollutants. In the present study, the effects of lead and mercury induced nephrotoxicity were studied in Wistar rats. Lead nitrate (LN, 45 mg/kg b.w/day) and mercury chloride (MC, 0.02 mg/kg b.w/day) and their combination were administered orally for 28 days. Four groups of rats were used in the study: control, LN, MC and LN plus MC groups. Serum biochemical parameters, lipid peroxidation, antioxidant enzymes and histopathological changes in kidney tissues were investigated in all treatment groups. LN and MC caused severe histopathological changes. It was shown that LN, MC and also co-treatment with LN and MC exposure induced significant increase in serum urea, uric acid and creatinine levels. There were also statistically significant changes in antioxidant enzyme activities (SOD, CAT, GPx and GST) and lipid peroxidation (MDA) in all groups except control group. In this study, we showed that MC caused more harmful effects than LN in rats.

Doxorubicin hepatotoxicity and hepatic free radical metabolism in rats. The effects of vitamin E and catechin.

Doxorubicin (DXR) is an anthracycline antibiotic, broadly used in tumor therapy. In the present study we investigated whether vitamin E and catechin can reduce the toxic effects of doxorubicin. Vitamin E (200 IU/kg/week), catechin (200 mg/kg/week), doxorubicin (5 mg/kg/week), doxorubicin+vitamin E (200 IU/kg/week), doxorubicin+catechin (200 mg/kg/week) combinations were given to rats weighing 210-230 g (n=6/group). Changes in major enzymes participating in free radical metabolism superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase (GSHPx), catalase (CAT) and malondialdehyde (MDA) were evaluated in the livers of all animals. Superoxide dismutase and catalase activity increased in the doxorubicin-treated group compared to control (P<0.05). Glutathione peroxidase levels increased in the catechin+doxorubicin-treated group (P<0.05) and reached maximum concentrations in the doxorubicin-treated group compared to control (P<0.01). Malondialdehyde levels increased in the doxorubicin-treated group compared to control and all-treated groups (P<0.05). Malondialdehyde, glutathione peroxidase and catalase activities were decreased in the vitamin E+doxorubicin- and catechin+doxorubicin-treated group compared to doxorubicin-treated group (P<0.05). All enzymes activities showed no statistical differences in the not mentioned groups above (P>0.05). Electron microscopic studies supported biochemical findings. We conclude that vitamin E and catechin significantly reduce doxorubicin-induced hepatotoxicity in rats.

Diazinon-induced hepatotoxicity and protective effect of vitamin E on some biochemical indices and ultrastructural changes.

Diazinon, an organophosphate insecticide has been used in agriculture and domestic for several years. The aim of present study was to analyze the hepatotoxic effect of diazinon which caused biochemical and ultrastructural changes in adult male Wistar rats and to evaluate the possible protective effect of vitamin E. Vitamin E (200 mg/kg, twice a week), diazinon (10 mg/kg per day, once a day in corn oil) and vitamin E (200 mg/kg, twice a week)+diazinon (10 mg/kg per day, once a day in corn oil) combination were given to rats (n=8) orally via gavage for 7 weeks. Biochemical indices in serum [total protein, albumin, alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol, triglyceride and low density lipoprotein cholesterol (VLDL-cholesterol)] and ultrastructural changes were investigated at the end of the 1st, 4th and 7th weeks comparatively with control group (n=8). It was observed that; at the end of 1st week, there was a statistically significance in all parameters except total protein and albumin, and at the end of 4th and 7th weeks, there was a statistically significance in all parameters when diazinon-treated group compared to control group (P<0.01). At the end of 1st week, ALP, ALT, total cholesterol and triglyceride, at the end of 4th week, all parameters except VLDL-cholesterol, at the end of 7th week, all parameters were statistically significant when vitamin E+diazinon-treated group compared with diazinon-treated group (P<0.01). In our electron microscopic investigations, while swelling of mitochondria and breaking up of the mitochondrial cristae of hepatocytes in diazinon-treated groups were observing, no pathological findings were observed in vitamin E+diazinon-treated groups. We conclude that vitamin E decreases diazinon hepatotoxicity, but vitamin E does not protect completely.

The effects of acarbose and Rumex patientia L. on ultrastructural and biochemical changes of pancreatic B cells in streptozotocin-induced diabetic rats.

This study was performed to observe the effects of acarbose and Rumex patientia on morphological change of pancreatic B cells in streptozotocin (STZ)-induced diabetic (type 2) rats. Two-day-old Wistar albino rats were intraperitoneally injected with 100mg/kg of STZ or vehicle alone for control. Vehicle and STZ given rats were divided into six groups (1st, 2nd and the 3rd groups are control; the 4th, 5th and 6th groups are STZ groups). The 1st and the 4th groups received water, the 2nd and the 5th groups received 40 mg acarbose/100 g feed, the 3rd and the 6th groups received 2% decoction of Rumex patientia grain. During experimentation period, blood glucose levels were checked periodically, and HbA1c level was measured from cardiac blood at the end of the experiment. Pancreas tissues were examined by electron microscope. Glucose and HbA1c levels increased by STZ were decreased by acarbose and Rumex patientia. Morphologically, we found a mitochondrial vacuolization and swelling as well as dilatation of the endoplasmic reticulum in the B cells of STZ-induced diabetic rats. Also, a decrease in the secretory granules of B cells was observed in the STZ-induced diabetic group. No pathological changes were observed in the STZ+acarbose group. In the STZ+Rumex patientia group, a weak swelling in the B cells was observed in the some of the mitochondria.

Effects of endosulfan on Thaumetopoea pityocampa (Lepidoptera: Thaumetopoeidae) larvae.

Thaumetopoea pityocampa larvae are very harmful to pines and they also cause allergic reactions in men and animals. In this study, different concentrations of endosulfan were administered to T. pityocampa larvae via pine needles which were prepared by the dipping method. The data obtained were statistically evaluated using probit analysis and a LC(50/48 hrs) value for T. pityocampa larvae found to be 1.679 mg/l. Also, 12, 24, 36 and 48 hrs after 1.679 mg/1 endosulfan treatment, ultrastructural changes in the midgut epithelium of T. pityocampa were investigated. No pathological changes were observed after 12 hrs, swelling and vacuolization of mitochondria and dilation ofendoplasmic reticulum after 24 hrs, swelling ofmitochondria and breaking of mitochondrial cristae and dissolving of nucleoplasm after 36 hrs, finally large vacuoles in the midgut epithelium cells were observed after 48 hrs.

Effects of lead nitrate and sodium selenite on DNA damage and oxidative stress in diabetic and non-diabetic rat erythrocytes and leucocytes.

The adverse effects of lead nitrate (LN) and the preventive role of sodium selenite were investigated in diabetic and non-diabetic rat blood by measuring trolox equivalent antioxidant capacity (TEAC), ferric reducing antioxidant power (FRAP), malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) also by evaluating DNA damage with comet assay. LN increased the levels of MDA, tail DNA%, mean tail length and tail moment, decreased the enzymes activities, FRAP and TEAC values. In sodium selenite+LN group, we observed the protective effect of sodium selenite on examining parameters. Diabetes caused alterations on these parameters, too. We found that sodium selenite did not protect against diabetes caused damages. As a result, LN caused toxic effects on blood cells and sodium selenite alleviated this toxicity but it did not show preventive effect against diabetes. Also, LN caused more harmfull effects in diabetic groups than non-diabetic groups.

Protective effects of sodium selenite on lead nitrate-induced hepatotoxicity in diabetic and non-diabetic rats.

In the present study, the effect of sodium selenite on lead induced toxicity was studied in Wistar rats. Sodium selenite and lead nitrate were administered orally for 28 days to streptozotocin induced diabetic and non-diabetic rats. Eight groups of rats were used in the study: control, sodium selenite, lead nitrate, lead nitrate+sodium selenite, streptozotocin-induced diabetic-control, diabetic-sodium selenite, diabetic-lead nitrate, diabetic-lead nitrate+sodium selenite groups. Serum biochemical parameters, lipid peroxidation, antioxidant enzymes and histopathological changes in liver tissues were investigated in all groups. There were statistically significant changes in liver function tests, antioxidant enzyme activities and lipid peroxidation levels in lead nitrate and sodium selenite+lead nitrate treated groups, also in diabetic and non-diabetic groups. Furthermore, histopathological alterations were demonstrated in same groups. In the present study we found that sodium selenite treatment did not show completely protective effect on diabetes mellitus caused damages, but diabetic rats are more susceptible to lead toxicity than non-diabetic rats.

Endosulfan-induced cardiotoxicity and free radical metabolism in rats: the protective effect of vitamin E.

Endosulfan is widely used in insect control and it is absorbed by both humans and animals through ingestion, inhalation and percutaneously. The aim of this work was to study antioxidant enzyme system which include superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) and malondialdehyde (MDA), the end product of lipid peroxidation and ultrastructural changes that might occur in the heart tissue of adult male Wistar rats as a result of endosulfan intoxication. Vitamin E (200 mg/kg, twice a week), endosulfan (2 mg/kg, per day, once a day in corn oil) and vitamin E (200 mg/kg, twice a week)+endosulfan (2 mg/kg, per day, once a day in corn oil) combination were given to rats (n = 10/group) orally via gavage for 6 weeks. SOD, GPx, CAT activities and MDA level increased in the endosulfan-treated group heart tissue compared to control group (P < 0.01, P < 0.01, P < 0.05 and P < 0.01, respectively). SOD, GPx activities and MDA level decreased in the vitamin E + endosulfan-treated group compared to endosulfan-treated group (P < 0.05, P < 0.05 and P < 0.05, respectively). Decrease of CAT activity was not significant statistically in the vitamin E + endosulfan-treated group compared to endosulfan-treated group. CAT activity increased in the vitamin E + endosulfan treated group compared to control group (P < 0.05). Increase of SOD, GPx activities and MDA levels were not significant statistically in the vitamin E + endosulfan-treated group compared to control group. In electron microscopic investigations while cytoplasmic edema and swelling and vacuolization of mitochondria of myocardial cells in endosulfan-treated group was observing, only a weak swelling of mitochondria of myocardial cells in vitamin E + endosulfan-treated group was observed. We conclude that vitamin E significantly reduce endosulfan-induced cardiotoxicity in rats.

Effects of endosulfan on B cells of Langerhans islets in rat pancreas.

Endosulfan is widely used in insect control and it is absorbed by both humans and animals through ingestion, inhalation, and percutaneously. The purpose of this work was to study blood glucose levels and ultrastructural changes that might occur in the pancreas of adult male Wistar rats as a result endosulfan intoxication. The treated group (n = 60) received endosulfan orally via gavage 2.0 mg/kg per day in corn oil for 6 weeks, while the control group (n = 10) was given equal amount of corn oil for the same period. The substances were administrated once a day. Blood glucose levels were significantly increased at the end of 3rd and 4th week (P < 0.05), and 5th and 6th week (P < 0.01) after administration of endosulfan to rats compared with the control group. In electron microscopy studies, at the end of 2nd and 3rd weeks, swelling of mitochondria; at the end of 4th week, vacuoles in cytoplasm; at the end of 5th week, dissolution of mitochondrial matrix; and at the end of 6th week, picnotic nucleus in B cells in Langerhans islet were observed after endosulfan treatment.