Oxidative stress by inorganic arsenic: modulation by thyroid hormones in rat (original) (raw)
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Influence of thyroxine and n-propylthiouracil on nephro-toxicity of inorganic arsenic in rat
Toxicology and industrial health, 2006
The effect of hyper or hypoactive thyroid on the renal toxicity of arsenic trioxide has been studied in rats. It was observed that pre-treatment of rats with thyroxine stimulates arsenic excretion in urine. The anti-thyroid drug n -propylthiouracil (PTU), inhibits the accumulation of arsenic in renal tissue. Both treatments affect the renal pathology. Histopathological lesions are less severe in PTU and arsenic-treated rats in comparison to thyroxine and arsenic-treated rats. Ultrastructural studies support light microscopical observations. An adaptive response was noticed against arsenic in PTU pre-treated rats. We attribute this response to decreased glutathione-S-transferase (GSH) activity and increased GSH synthesis in the kidney. A relationship between thyroidal activity and arsenic toxicity is suggested by present observations. Toxicology and Industrial Health 2006; 22: 137 Á/145.
Metabolic adaptations to arsenic-induced oxidative stress in male wistar rats
Journal of Biochemical and Molecular Toxicology, 2012
The present study was planned to investigate the effect of arsenic in rats on several biochemical indices of oxidative stress. Rats were exposed to arsenite in drinking water for upto 12 weeks. Chronic exposure to arsenic for a period of 12 weeks significantly ( p < 0.05) increased arsenic burden in blood, liver, and kidney. Several intrinsic antioxidant defenses were activated after a 4-week exposure to arsenic. Some remained elevated, but others became depressed over a longer exposure period. Alterations in most of the biochemical variables reached statistical significant ( p < 0.05). Arsenic significantly ( p < 0.01) reduced mRNA expression of the superoxide dismutase 2 (SOD2) gene with respect to the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) gene. These observations indicated that prolong exposure to arsenic causes induction of oxidative stress and biochemical alterations. C 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:109-116, 2012; View this article online at wileyonlinelibrary.com.
Pharmacology & Toxicology, 1996
Adult male rats were treated orally with sodium arsenate (10 mg As/ kg/day) for 2 days, and an increase in hepatic glutathione level was seen. Ascorbic acid content increased in both liver and plasma of intoxicated animals. Hepatic activities of superoxide dismutase and glutathione peroxidase did not change with the treatment and there was no increase in the level of lipid peroxidation measured as thiobarbituric acid-reacting substances (TBARS). Arsenic decreased the plasma level of uric acid and increased the plasma triglycerides content without modifying vitamin E levels. Both total lipoproteins and very low density lipoprotein plus low density lipoprotein (VLDL+ LDL) fractions demonstrated greater propensity for in vitro oxidation than the corresponding untreated rats. The last finding might be a useful parameter for determining the degree of oxidative stress in the initial steps of intoxication with arsenic. Arsenic is the twentieth most abundant element in the earth's crust and is present in all living organisms. Drinking water usually contains a few micrograms of arsenic per liter or less, but higher concentration have been reported from various mineral springs, e.g. Japan (1.7 mg A d) , Cordoba, Argentina (3.4 mg A d) and Taiwan (1.8 mg A d) (Goyer 1991). The trivalent compounds of arsenic are the principal toxic forms (Ochi et al. 1994), but chronic poisoning with drinking water has been reported (Cebrian et al. 1983). In this case the arsenic was present mainly in the pentavalent form. The potential carcinogenicity of arsenic has been extensively reviewed (WHO 1981; U.S.Environmenta1 Protection Agency 1987). Chronic exposure to the inorganic arsenic compounds may lead to neurotoxicity, hepatic injury and peripheral vascular disease, but there are no specific biochemical parameters that reflect arsenic toxicity (Goyer 1991). Hence, this study was planned to investigate the effect of sodium arsenate on the host hepatic antioxidant defense systems, oxidative stress status and other biochemical parameters. Materials and Methods Animals. Adult male rats (Wistar strain) weighing between 200-250 g were divided randomly into two groups of six animals each and housed in well ventilated cages at room temperature (22k2") and a relative humidity of 50-60%. The animals had free access to tap water and food from a standard laboratory diet.
Oxidative stress in liver of mice exposed to arsenic-contaminated water
Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
Oxidative stress has been implicated in the initiation of hepatic damage caused by various agents. Not much data on oxidative stress in liver in chronic arsenic exposure are available in the literature. We therefore studied this aspect in a murine model. BALB/c mice were given arsenic-contaminated (3.2 mg/L) or arsenic-free (< 0.01 mg/L, control) drinking water ad libitum. Batches of mice were sacrificed after 2 and 4 months, and blood samples and liver tissue were collected. Liver histology was examined and levels of hepatic reduced glutathione (GSH), malondialdehyde, and enzymes of the antioxidant defense system in the liver tissue were determined. Arsenic content in liver tissues obtained at 4 months was estimated. Two-month exposure to arsenic caused significant elevation of hepatic GSH (11.4 [0.8] micrograms/mg protein) compared to control mice (9.3 [0.4]; p < 0.01). Levels of enzymes related to GSH homeostasis were also elevated. At 4 months, hepatic GSH was significantl...
PloS one, 2024
Arsenic has been identified as an environmental toxicant acting through various mechanisms, including the disruption of endocrine pathways. The present study assessed the ability of a single intraperitoneal injection of arsenic, to modify the mRNA expression levels of estrogen-and thyroid hormone receptors (ERα,β; TRα,β) and peroxisome proliferator-activated receptor gamma (PPARγ) in hypothalamic tissue homogenates of prepubertal mice in vivo. Mitochondrial respiration (MRR) was also measured, and the corresponding mitochondrial ultrastructure was analyzed. Results show that ERα,β, and TRα expression was significantly increased by arsenic, in all concentrations examined. In contrast, TRβ and PPARγ remained unaffected after arsenic injection. Arsenic-induced dose-dependent changes in state 4 mitochondrial respiration (St4). Mitochondrial morphology was affected by arsenic in that the 5 mg dose increased the size but decreased the number of mitochondria in agoutirelated protein-(AgRP), while increasing the size without affecting the number of mitochondria in pro-opiomelanocortin (POMC) neurons. Arsenic also increased the size of the mitochondrial matrix per host mitochondrion. Complex analysis of dose-dependent response patterns between receptor mRNA, mitochondrial morphology, and mitochondrial respiration in the neuroendocrine hypothalamus suggests that instant arsenic effects on receptor mRNAs may not be directly reflected in St3-4 values, however, mitochondrial dynamics is affected, which predicts more pronounced effects in hypothalamus-regulated homeostatic processes after long-term arsenic exposure.
Advances in Life Science and Technology, 2019
Arsenic is an environmental pollutant and its contamination in the drinking water is considered as a serious worldwide environmental health threat. The present study investigated the effects of arsenic exposure on antioxidant parameters and p53 expression in male albino rats. The animals (n=45) were exposed to arsenic (100 ppm, 150 ppm and 200 ppm) for 4, 8 and 12 weeks as sodium arsenate in drinking water. Control animals (n=15) received distilled water for the same period. Hepatic superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), reduced glutathione (GSH), lipid peroxidation and total protein were evaluated spectrophotometrically. Expression of p53 was also detected by histochemical staining. Before the commencement of arsenic exposure, five animals were sacrificed to obtain baseline data. ANOVA followed by Tukey's test was used to analyse the results with p<0.05 considered significant. Significant decrement in hepatic activities of SOD, catalase and GPx as well as hepatic concentration of GSH and total protein concentration characterized exposure to all the dose regimens of inorganic arsenic at all the time interval. Corroboratively, significant elevation was observed in malondialdehyde (MDA). The expression of p53 decreased in the groups that were exposed to arsenic as compared to the control animals. The findings from the present study suggests excessive generation of free radicals and reduction in p53 expression in arsenic-induced hepatotoxicity.
Veterinarski arhiV, 2008
In this experiment thirty rats were exposed to 0 (Gr. I, healthy controls) or 10 ppm arsenic (sodium arsenite) through drinking water ad lib for eight weeks after dividing them into five groups of six rats each. Rats in Gr. III, IV and V were administered a daily oral dose of cysteine, methionine or ascorbic acid 25 mg/kg body mass respectively, while those in Gr. II served as the treated control. At the end of the experimental period oxidative stress indices viz. lipid peroxides level (LPO), superoxide dismutase (SOD) and catalase (CAT) activities were estimated in blood, liver and kidneys from sacrificed rats. Arsenic exposure resulted in a significant (P<0.05) rise in LPO levels and activities of SOD and CAT in erythrocytes, liver and kidneys. All the different treatments reduced lipid peroxides levels and restored activities of antioxidant enzymes to variable extents in various tissues. However, arsenic exposure did not show any significant (P>0.05) effects on the body mass of rats of different groups over time. It is concluded from the present study that prophylactic co-administration of cysteine, methionine and ascorbic acid could provide tissue specific protection from oxidative injury during sub-chronic exposure to arsenic.
Arsenic and It's Adjuvantic Role on Oxidative Stress in Animals: A Brief Overview
Arsenic (As) exposure is a global public health problem because of its association with various cancers and numerous other pathological effects, and millions of people worldwide are exposed to As on a regular basis mainly through drinking water. Increasing lines of evidence indicate that As may adversely affect the antioxidant defense system, but its specific mechanism to abrupt the antioxidant defense system are poorly understood. Therefore, we conducted a literature search of As and its oxidative stress-related effects associated with As exposure and summarized the known oxidative disorders of As in humans and laboratory animals. Overall, the review indicates that chronic exposure to As has the potential to impair the antioxidant system which could lead to increased risk of disorders and chronic diseases, including various cancers. Further investigation, particularly in humans, is needed to better understand the relationship between As exposure and the development of disease as well as the proper mechanism.
Biochemical and histological alterations in liver following sub chronic exposure of arsenic
2015
Objective: Contamination of groundwater with arsenic is of global concern . The present work was aimed to evaluate the biochemical and histological changes in liver of female rats induced by sodium arsenite at doses naturally found in groundwater of Punjab. Method: Twenty four female rats were divided into four groups of 6 animals each. Group I animals received distilled water and served as control; Group II-IV received arsenic at the dose of 10, 30 and 50 ppb ( µg/L) dissolved in distilled water ad libitum for 30 days. At the end of experiment, animals were sacrificed and liver was collected for biochemical and histological evaluation. Results: Biochemical analysis showed an increase in the activity of hepatic marker enzymes including transferases, phosphatases and lactate dehydrogenase (LDH). Also, the levels of antioxidant enzymes (catalase, reduced glutathione and glutathione-S-transferase) decreased significantly (P<0.05) in treated animals when compared to control. A signif...