Effect of malathion on reproductive system of male rats

The pesticides are one of the most potentially harmful chemicals liberated in the environment in an unplanned manner Malathion is widely used as a potent pesticide in many countries and has been shown to produce some adverse health effects. A study was conducted to asses the effects of malathion on the male reproductive system of wistar rats. The pesticide was administered to rats orally at dose levels of 50, 150 and 250 mg/kg/body wt/day for 60 days. In comparison to the control rats, there was a significant reduction in the weight of testes, epididymis, seminal vesicle and ventral prostate. Testicular and epididymal sperm density were decreased in the animals treated with malathion. Pre and post fertility test showed 80% negative results after treatment Biochemical profile of the testis revealed a significant decline in the contents of sialic acid and glycogen. Whereas a significant increase in the protein content of testis and testicular cholesterol was observed. The activity of testicular enzyme acid phosphatase increased significantly while decreased alkaline phosphatase activity was found. Malathion also suppressed the level of testosterone significantly Results of the present study clearly suggest that malathion induce toxic effects on the male reproductive system of rats.     

Sub-lethal toxic effects of deltamethrin on blood biochemical parameters of Japanese quail,Coturnix japonica

Feeding deltamethrin-contaminated grains to domestic poultry, such as quails may result in toxic effects in these birds. This study was done to investigate the effects of recommended doses of deltamethrin, sometimes used in grain storage silos, on Japanese quail (Coturnix japonica). Quails were fed grains contaminated with 0.25 and 0.50 mg deltamethrin per kg diet for 21 days and the effects on survival and blood biochemical parameters were studied. Plasma uric acid, creatinine levels, and creatinine phosphokinase activity in the blood were increased. Aspartate aminotransferase and lactate dehydrogenase activities and glucose levels significantly increased in birds treated with the high dose of deltamethrin. Alanine aminotransferase activity and albumin or cholesterol levels were not changed, and acetylcholinesterase and alkaline phosphatase activities, total protein and globulin in plasma were decreased. Administration of 0.25 mg/kg deltamethrin caused increased blood triglyceride levels, 0.50 mg/kg deltamethrin decreased triglyceride levels.     

Pre-administration of beta-carotene protects tissue glutathione and lipid peroxidation status following exposure to gamma radiation

The present study has been aimed to investigate the protective effect of beta-carotene against radiation-induced oxidative stress in mice tissues using lipid peroxidation and glutathione (GSH) as end points. Fourteen days oral priming administration of beta-carotene (35 mg/kg body weight) followed by an acute dose of gamma radiation (5 Gy) inhibited the augmented level of thiobarbituric acid reactive substance (TBARS) and a statistically significant protection against GSH depletion. Results evaluated from this study clearly indicate the antioxidative property of beta-carotene against gamma radiation, which is suggestive of free radical scavenging and singlet oxygen quenching.     

Hepatoprotective effects of taurine against mercury induced toxicity in rats

An attempt has been made to study the influence of taurine on mercury intoxicated rats. The animals were treated with sublethal dose of mercuric chloride (2 mg/kg body wt.) for 30 days. During the mercury treatment, the level ofAspartate transaminase(AST), Alanine transaminase (ALT) and Alkaline phosphatase(ALP) in serum and lipid peroxidation (LPO) in liver tissue significantly increased whereas Glutathione (GSH), Glutathione peroxidase(GPx), Catalase (CAT) and Superoxide dismutase (SOD) were simultaneously decreased in the liver tissue. Present results indicate that the liver tissue was completely damaged, after mercury treatment. In another group of animals, taurine (5 mg/kg body wt.) was administrated for another 15 days. Taurine administration was observed to improve the liver function in mercury intoxicated animal as indicated by the decline in increased levels of AST, ALT and ALP in serum and LPO content in liver tissue. The decreased level of antioxidant system (GSH, GPx, CATand SOD) has been promoted Results suggested that taurine played a vital role in reducing the mercury toxicity in intoxicated animals.     

Hepatotoxic and haematological effects of Nigerian Bonny light crude oil in male albino rats

The effect of Bonny light crude oil was assessed in adult albino rats. The rats were administered with 200, 400, and 800?mg/kg of the crude oil orally for 7 days. Fluid intake was measured daily, and the initial and final animal body weight recorded. Oral crude oil at these doses produced no effect on feed and fluid intake between the test groups and the control group. There was a significant decrease in body weight compared to the control group after 7 days of treatment with the different doses of crude oil.

The toxic effects of the liver and hematological effects were assessed. The packed cell volume (PCV) and total white blood cell (WBC) of the 200?mg/kg group were significantly decreased compared to the respective control values. Administration of 200, 400, and 800 mg/kg of Bonny light crude oil, caused a significant dose-dependent increase in glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels, but a significant decrease in the alkaline phosphatase (AP) level compared to the control. Histological examination indicates that crude oil induced severe pathologic changes in the forms of necrosis and oedema.     

Protective efficacy of Mucuna pruriens extract on Epichlorohydrin induced toxicity in epididymis of albino rats

The protective effects of seeds of Mucuna pruriens on epichlorohydrin (ECH)-induced toxicity in epididymis and epididymal sperms of rats were studied. Different doses of ECH and M. pruriens (75 and 100 mg kg^?1, respectively) were administered daily, orally for 70 days. Group I animals served as control. Group II and III rats received ECH (75 or 100 mg kg^?1 body weight, respectively) alone. The group IV and V rats received a combination of both ECH and the seed extract of M. pruriens at 75 or 100 mg kg^?1 body weight. Group VI rats was administered only the extract of M. pruriens 100 mg kg^?1 body weight. At the end of the experiment (71st day), rats were sacrificed and sperm collected from epididymis were used for the assessment of sperm count, sperm viability, and sperm motility. Administration of ECH produced a reduction in epididymal sperm count, sperm viability, and sperm motility. The activities of catalase, superoxide dismutase, and glutathione peroxidase were decreased, while lipid peroxidation was increased. ECH produced a decrease in the levels of protein, acid phosphatase, sialic acids, and increased the level of alkaline phosphatase, and cholesterol. The administration of M. pruriens to ECH-treated rats resulted in a protective effect.     

Evaluation of reproductive and developmental toxicity of cypermethrin in male albino rats

The ever-increasing use of pesticides in the agricultural and public health has become a major cause of sterility in human and various other animals particularly in males. This study was sought to screen the toxic impacts of cypermethrin (synthetic pyrethroid) on reproduction and development. Twenty-four Wistar male rats divided into four groups were orally administered cypermethrin of daily doses 50, 75, or 100 mg?kg^?1 bwt per day for 45 days; and for developmental toxicity, 12 female rats were separated into two groups. Maternal rats (experimental) were administered cypermethrin (100?mg?kg^?1) by gavage daily from 6th to 17th day of gestation, and the control group was dosed only vehicle (olive oil). The body weights, fertility index, biochemical, enzymatic, hormonal, and histopathological parameters were the criteria used to evaluate the toxicity of cypermethrin. Study showed significant decline in the weight of testes, epididymises, seminal vesicles, and ventral prostate, and reduction in sperm counts both in epididymises and testes in chemical-treated animals. Pre- and post- fertility test showed 50%, 80%, and 100% negative results after treatment. A significant degenerative reduction in testicular glycogen and sialic acid was also noted. In contrast, protein and cholesterol levels of testes were significantly increased. In addition, acid phosphatase activity was significantly increased, while alkaline phosphatase, testosterone, leutinizing hormone (LH), and follicle stimulating hormone (FSH) levels were diminished. Histology of testes showed degenerative changes in seminiferous tubules. Cypermethrin exposure during gestation produced adverse effects markedly in females and fetuses.     

Biochemical and histopathological ultrastructural changes caused by ZnO nanoparticles in mice

Five week-old mice were divided into a vehicle control group, and groups exposed to ZnO nanoparticles at low (0.5 g/kg), middle (1 g/kg), high (3 g/kg), and exceptionally high-dose (5 g/kg). After the first, second, third, and fourth weeks’ of exposure, blood biochemistry, histopathology, and electron microscopic ultrastructural changes in liver, kidney and spleen were investigated. Increased alkaline phosphatase activities were observed in all treated mice being statistically significant at higher dose. No changes were observed in the serum glutamic pyruvic transaminase, serum glutamic oxaloacetic transaminase, creatinine, blood urea nitrogen, and lipid levels. During the first and second weeks of the treatment, effects on the cytoarchitecture of liver, kidney, and spleen were not perceived while during the third and fouth weeks of treatment sporadic mild effects were seen. Ultrastructural electron microscopic changes in liver, kidney, and spleen were not observed for the low-dose group on the first, second, third, and fourth weeks, suggesting that exposure to ZnO nanoparticles at low dose is safe. Long-term (i.e., more than 28 days) exposure to the exceptionally high-dose resulted in sporadic changes in nuclear chromatin condensation, irregular nuclear membrane, polymorphic mitochondria, mitochondrial swelling, and vacuolation. ZnO nanoparticles could be well tolerated and no death occurred in any group of treated mice.     

Role of GSH in the amelioration of chromium-induced membrane damage

Membrane damage is one of the important consequences of chromium (Cr), an environmental toxicant, induced cytotoxicity. Reduced glutathione (GSH), a membrane protectant may be used to reduce the Cr-induced membrane damage. In the present study, the impact of Cr in presence and absence of GSH was studied on plasma membrane of the liver and kidneys in male Wistar rats. Significant increases in membrane cholesterol levels as well as significant decreases in membrane phospholipid levels in Cr exposed (0.8 mg per 100 g body weight, i.p., for 28 days) animals suggest structural alterations in both the liver and kidney plasma membranes. Alkaline phosphatase (ALP), total ATPase, and Na⁺–K⁺–ATPase activities of plasma membrane were significantly decreased in both the liver and kidneys after Cr treatment. This treatment also produced significant weight loss and increased Cr content in the liver and kidneys. However, GSH (8 mg per 100g body weight, i.p., daily at an interval of 6 h after injection of Cr for a period of 28 days) supplementation restored alterations induced by Cr in plasma membrane of both the liver and kidneys but was not able to eliminate the deposited Cr from the liver and kidney tissues.     

Biochemical evaluation of hepatotoxicity in mice due to administration of artemether

Effects of artemether administration on liver and selected biochemical parameters were evaluated. Eighty albino mice were divided into four equal groups. Group 1 was given water which served as control, while groups 2, 3, and 4 were given 1.2, 2.4, or 4.8 mg kg^?1 body weight artemether intramuscularly for five consecutive days. On day 6 all mice were sacrificed by cervical dislocation and blood was collected for analysis of alanine and aspartate transaminases, alkaline phosphatase, copper, and total proteins. Liver tissues were prepared for histological studies. It was found that the serum alanine and aspartate transaminase and alkaline phosphatase activities were higher in groups treated with artemether compared to control. The serum concentrations of copper and total proteins were lower than control. The histological features of liver tissues after administration of artemether showed histopathological alterations. These findings showed that artemether administration may have reversible adverse effects on mouse hepatocytes.     

Potential hepatoprotective effects of vitamin E and Nigella sativa oil on hepatotoxicity induced by chronic exposure to malathion in human and male albino rats

Malathion is an organophosphorus (OP) insecticide and has a wide range of use in agriculture, veterinary medicine, and public health. Malathion and other OP insecticides produce hepatotoxic effects. The objective of the present study was to investigate the protective effects of Nigella sativa oil and α-tocopherol (vitamin E) on the hepatotoxicity induced by malathion on workers involved in the formulation of pesticides, chronically exposed to malathion, and in male albino rats orally administrated malathion. This study was conducted on both human and experimental animals, the human study was conducted on 30 control subjects working as administrators and 45 subjects working in formulation of pesticides and exposed to malathion (≥3 years), all were males with age ranges from 30 to 60 years. The 45 males working in pesticides formulation were classified into three groups; (1) 15 workers exposed to pesticides (2) 15 workers exposed to pesticides and received vitamin (E), in a dose of 10 mg kg?1 day^?1 orally for 60 days, and (3) 15 workers exposed to pesticides and received 100 mg kg^?1 day^?1 of N. sativa oil for 60 days. The animal experiment was conducted on 40 adult male albino rats weighing 150–200 g. They were divided into four groups (10 rats in each group). First group served as the control group, the second group received malathion in a dose of 50 mg kg^?1 orally per day for 60 days, the third group received malathion (in the same dose and route of administration) and vitamin E in a dose of 10 mg kg^?1 day^?1 orally for 60 days, and the fourth group received malathion (in the same dose and route of administration) and N. sativa oil in a dose of 100 mg kg^?1 day^?1 orally for 60 days. Liver function tests (alanine aminotransferase [ALT], aspartate aminotransferase [AST], serum alkaline phosphatase [ALP], albumin, globulin, albumin/globulin ratio, and total proteins), antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD), and total glutathione peroxidase (GPx)), and lipid peroxidation [MDA] were analyzed in both human and animal experiments. The results of both human and animal study revealed that, exposure to malathion produced significant increases in AST, ALT, and lipid peroxidation. There were significant decrease in albumin, albumin/globulin ratio, total protein, and antioxidant enzymes. There was no significant change in ALP. In addition exposed workers showed significant decreases in serum globulin. Nigella sativa oil or vitamin E administration showed significant improvement of liver function tests, lipid peroxidation, and antioxidant enzymes impairment induced by malathion. Thus, dietary supplement, N. sativa oil, or vitamin E may represent a potential therapeutic agent in reducing malathion-induced hepatotoxicity.     

多拷贝表达转鲑鱼降钙素基因酵母的急性、亚急性毒性

口服转鲑鱼降钙素基因酵母为鲑鱼降钙素的应用开辟了一条新的途径.为评价转鲑鱼降钙素基因酵母的安全性,将转基因酵母分别灌胃昆明种小鼠和Wistar大鼠进行急性毒性实验(7 d)、亚急性毒性实验(8周).急性毒性实验结果表明灌喂转基因酵母对小鼠无致死效应(LD50>10 000 mg/kg);亚急性毒性实验中高(2.0 g/kg)、低(0.5 g/kg)剂量组动物的一般状况、体重、主要脏器系数、血液学指标及血液生化指标与各对照组比较,均未见明显差异(P>0.05),组织病理切片检查未发现病理性变化.实验结果说明转鲑鱼降钙素基因酵母不会对实验动物造成不良影响,是安全无毒的.图3表3参16     

The role of thymoquinone as antioxidant protection on oxidative stress induced by imidacloprid in male and female Swiss albino mice

The aim of the present study was to evaluate the possible protective effects of thymoquinone (TQ), an antioxidant agent, against imidacloprid (IMI)-induced oxidative stress in male and female mice. In total, 48 Swiss Albino male and female mice were fed a standard rodent diet and divided into 3 equal groups: the animals in the control group (vehicle treated) were given corn oil, the second group were orally administered 15 mg/kg/day IMI alone, and the third group were orally administered 15 mg/kg/day IMI and with TQ at 10 mg/kg/day for 21 days. During the experimental period, there were no significant changes between initial body weights and final body weights of IMI treated male and female mice. IMI produced significant increase in blood, liver, kidney, and heart malondialdehyde (MDA) levels and decrease in blood and liver glutathione (GSH) levels. In addition, IMI treatment decreased erythrocyte, liver, and kidney superoxide dismutase (SOD) activity in male mice and decreased erythrocyte and liver SOD activity in female mice. Erythrocyte catalase (CAT) activities were found to be low in male and female mice. However, treatment with TQ reversed IMI-induced oxidative stress, lipid peroxidation, and activities of antioxidant enzymes. Moreover, TQ exhibited protective action against the IMI-induced histopathological changes in tissues of male and female mice. In conclusion, TQ was found to be effective in protecting mice against IMI-induced oxidative stress by enhancing antioxidant defense mechanisms.     

Hepato and nephrotoxicity in rat exposed to endosulfan

The indiscriminate and injudicious use of pesticides particularly endosulfan in agriculture and animal husbandry practices has considerably increased the risk of human health hazard. The present work was therefore undertaken to evaluate the toxic effect of endosulfan on the vital organs viz. liver and kidney of rat. Oral administration of endosulfan at the dose level of 10 mg/kg b.wt./day for two and four weeks showed toxic interference with the biochemistry and histology of rat liver and kidney. The biochemical parameters viz. Aspartate amino transferase, alanine amino transferase, acid phosphatase, alkaline phosphatase, bilirubin urea and creatinine were increased which clearly showed the hepato and nephrotoxic effect of endosulfan. Histopathologically the size of liver was increased, sinusoidal dilation, pyknotic nuclei, cytoplasmic degranulation and various nuclear aberrations were observed. Similarly pathological alterations viz. chronic glomerulonephritis, glomerulosclerosis, odenoma and glomerulus deposits were observed in the kidney.     

Chronic study of arsenic trioxide-induced hepatotoxicity in relation to arsenic liver accumulation in rats

This study measured activities of serum enzymes alkaline phosphatase, acid phosphatase, glutamic oxaloacetic transaminase (SGOT), and glutamic pyruvic transaminase (SGPT), markers of liver function in albino rats after continuous ingestion of arsenic trioxide (As₂0₃). For the study, treated animals were given AS₂O₃ (0.2 mg/100 g/day) orally for 180 days. After the completion of treatment, the blood was collected for the estimation of serum biochemical markers. The results obtained were compared with control group. Data showed a significant increase in SGOT and SGPT activity after 60 days of As₂0₃ administration. The level of alkaline phosphatase and acid phosphatase increased significantly after 90 and 120 days, respectively. Since the elevation of these serum enzymes is an indicator of hepatic damage, data indicate that As₂O₃ produces hepatotoxicity. When taken continuously, arsenic was also deposited in liver and blood and affected the enzymatic pathways. Total accumulated arsenic was determined by HG-AAS at 193.7 nm.     

邻苯二甲酸二乙基己酯(DEHP)对小白鼠肝脏毒性及脂质过氧化损伤

为研究邻苯二甲酸二乙基己酯(DEHP)对小鼠肝脏的毒性及脂质过氧化损伤作用机制,选择昆明4周龄小鼠80只,雌雄各半,随机分为4组。经食饵连续自然给食染毒,于染毒第4周末处死。测量小鼠肝脏和体重的变化,测定不同DEHP染毒剂量组小鼠的血液、肝脏中谷胱甘肽过氧化物酶(GPX)、过氧化氢(H2O2)和丙二醛(MDA),超氧化物歧化酶(SOD)的变化。将实验数据进行ANO-VA分析处理。结果表明,随着染毒剂量的增加,小鼠体重逐渐减少(p<0.01),高剂量组肝脏器系数明显上升(p<0.01)。苏木精-伊红染色法(简称HE染色)可见高剂量组肝脏组织有明显损伤。与对照组相比,DEHP3个剂量染毒组小鼠血液(75mg·kg-1组除外)及肝脏中GPX活性降低(p<0.05,p<0.01),H2O2含量增加(p<0.05,p<0.01);肝组织中(75mg·kg-1组除外)SOD活性降低(p<0.05,p<0.01),MDA含量增加(p<0.01)。以上结果说明DEHP对小鼠肝脏的毒性作用机制可能为脂质过氧化反应。     

Biochemical and histological alterations induced by a formulation of dicofol in the embryonic liver of Gallus domesticus

In the present investigation, hepatotoxic effect of a commercially available insecticide formulation of dicofol (Colonel–S® 18.5% emulsified concentrate) was studied in the developing chick embryo. Fertilized eggs of Gallus domesticus were immersed in three different dose concentrations, i.e. 250, 500, and 1000 mg L^?1 of Colonel–S on “0” and fourth days of incubation for 60 min at 37 °C and incubated till embryonic day 16. Severe histopathological cellular lesions, such as extensive cell degeneration and necrosis with enlarged blood sinusoids, cytoplasmic vacuolization, and leucocyte infiltrations with congestion or dilation of central vein, appeared in dose-depended manner. Dicofol treatment also caused significant decrease in the levels of total protein, glycogen, and glutathione content and an increase in alkaline phosphatase activity of embryonic liver, whereas glutamic pyruvic transaminase activity showed mixed response.     

Adverse effects of mercuric chloride on thyroid of mice, Musculus albinus and pattern of recovery of the damaged activity

The protective role of "essentiale phospholipids" (EPL) on mercury induced thyroid dysfunction with special reference to cholesterol, thyroid peroxidase and thyroxine activity in mice were investigated. The animals were treated with 0.5 ml/day of 0.5 ppm aqueous mercuric chloride for a period of 7, 14 and 21 days. For the recovery 175 mg of EPL was given to mice (already treated with HgCl2) for a period of 7, 14 and 21 days. Daily treatment of HgCl2 for 7, 14 and 21 days decreased serum cholesterol, TPO and T4 activity. Simultaneous administration of EPL (25 mg/mice) restored thyroid function in mice by maintaining serum thyroid hormone concentration almost normal. It increased serum cholesterol, TPO and T4 activity. It appears that the protective effect of EPL against HgCl2 induced thyroid dysfunction is mediated through its antioxidative action.     

Toxicity of Nerium oleander leaf extract in mice

Non-lethal dose of 70% ethanol extract of the Nerium oleander dry leaves (1000 mg/kg body weight) was subcutaneously injected into male and female mice once a week for 9 weeks (total 10 doses). One day after the last injection, final body weight gain (relative percentage to the initial body weight) had a tendency, in both males and females, towards depression suggesting a metabolic insult at other sites than those involved in myocardial function. Multiple exposure of the mice to the specified dose failed to express a significant influence on blood parameters (WBC, RBC, Hb, HCT, PLT) as well as myocardium. On the other hand, a lethal dose (4000 mg/kg body weight) was capable of inducing progressive changes in myocardial electrical activity ending up in cardiac arrest. The electrocardiogram abnormalities could be brought about by the expected Na+, K(+)-ATPase inhibition by the cardiac glycosides (cardenolides) content of the lethal dose.     

Occupational exposures,delivered doses and exposure limits for chromium and nickel†

The interaction of HCH (50 mg/kg) and dietary protein levels on microsomal drug metabolizing enzymes system and liver lipids were studied in the rats for 90 days. The results indicated that rats fed a lower protein diet and HCH has a higher rate of mortality, lower rate of growth and an increased liver weight. A significant induction in the hepatic microsomal aminopyrine‐N‐demethylase, p‐nitroanisole‐O‐dealkylase, benzo(a)pyrene hydroxylase and glutathione‐S‐transferase activity was observed in pesticide treated animals as compared to control animals. The pathological changes observed in liver of HCH treated animals consisted mainly of necrosis and fatty degeneration of hepatocytes. HCH also induced the significant accumulation of cholesterol, triglycerides, phospholipid and total lipid in liver in low protein diet animals. Protein accelerates the metabolism of HCH, resulting in a decrease of HCH concentration with the increase of dietary protein level. A close correlation existed between lipid accumulation, induction of drug metabolizing enzyme system and deposition of HCH in liver.