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Introduction: The impact of chromium exposure was studied on liver, kidney, testis, spleen, cerebrum and cerebellum of male Wistar rats (80-100 g body weight).
Material & Method: It was observed that treatments of rats with chromium (i.p. at a dose of 0.8 mg / 100 g body weight per day) for a period of 28 days caused significant increase in chromium content while declining the body weight along with the organ weight, except liver.
Results: Decreased acid phosphatase (ACP) and alkaline phosphatase (ALP) activities were observed in most of the organs. Significant increases in the cholesterol contents of all the organs were associated with the significant decreases in the level of phospholipids. Lipid peroxidation decreased in liver and kidney while it increased in testis, cerebrum and cerebellum. Reduced glutathione (GSH) level was found to be increased in liver, spleen and cerebrum, and decreased in kidney and testis. Catalase activity became elevated in liver, kidney, spleen and cerebellum while it decreased in testis.
Conclusion: It is suggested that chromium treatment at the present dose and duration induces general tissue toxicity by causing membrane damage due to changes in the relative proportion of cholesterol and phospholipids in the membrane structure. In addition, tissue specific toxicity is affected by lipid peroxidation in testis, cerebrum and cerebellum, and in other tissues increased GSH level or enhanced catalase activity prevents lipid peroxidation to occur due to reactive oxygen species produced from chromium transformation.

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Background: Phthalates are a group of multifunctional chemicals. Diethyl phthalate (DEP) is one of the most frequently used phthalates in solvents and fixatives for numerous industrial products.
Method: The present experiment was designed to assess oxidative stress, if any, caused by diethyl phthalate. For this the homogenates of liver and kidney were treated with different concentrations ( 10-40 µg/mL) of DEP. 10% liver and kidney homogenates were prepared in phosphate buffered saline and used for estimation of lipid peroxidation.In final step lipid peroxidation and total protein content were analyzed.
Results: The result revealed significant and dose - dependent increase in lipid peroxidation, whereas protein content reduced significantly. Maximum increase in LPO and decrease in protein content was observed at 40 µg/mL of DEP concentration.
Conclusion: From this study, it can be concluded that different concentrations of DEP leads to dose- dependent significant increase in lipid peroxidation and decrease protein content.So at the different concentration of DEP cause oxidative stress.

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Background: Many health problems are related to lifestyle and dietary factors. Since ancient times, food additives such as sulfites have been used to preserve foods. Diverse effects of sulfites on multiple organs have been reported but its effect on female reproductive organ has not been fully elucidated. The aim of this study was to investigate the effects of sodium metabisulfite (SMB) on ovarian tissue in adult rats.

Methods: Four groups of female rats (n=32) were used. The experimental rats received 10, 100 and 260 mg/kg SMB for 28 days (S10, S100 and S260 groups, respectively). The control rats received distilled water for the same period. The ovarian volume, weight and the number of different types of follicles were estimated by stereological methods. Lipid peroxidation is assessed indirectly by the measurement of malondialdehyde (MDA), using the thiobarbituric acid (TBA) method.

Results: The results showed a significant decrease in the ovarian volume, the number of primordial, primary, secondary, grafian follicles and corpus luteum in the SMB-treated animals compared with the control group (P < 0.05). In comparison to the control group, the number of atretic follicles increased in the SMB-treated rats. MDA was significantly increased in S260 group compared to the control group.

Conclusion: The present data confirm sulfite-induced structural changes in the ovary. Increased level of MDA because of SMB ingestion suggests that free radicals may have a critical role in these changes.

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Background: The mechanism of cadmium induced osteoporosis is not well understood, so in this study, we examined the toxicity of bone marrow mesenchymal stem cell (MSCs) following treatment of rats with CdCl₂ in drinking water, to revile the effect of this chemical on differentiation potential of MSCs.

Methods: At the end of third passage, MSCs were grown in the osteogenic medium for 21 days. To study the differentiation property the viability, morphology, intracellular calcium, and matrix mineralization via quantitative alizarin red were evaluated. Besides, biochemical parameters including activity of alkaline phosphatase (ALP), aspartate amino transaminase (AST), alanine amino transaminase (ALT) as well as antioxidant enzyme such as superoxide dismutase, catalase, and peroxidase were determined too. In addition, level of lipid peroxidation based on determination of malondialdehyde (MDA) content was studied.

Results: The results showed significant reduction in the viability of cells after differentiation compared to control (P<0.05). The treatment of rats caused significant reduction in nuclear diameter. There was significant increase in (ALT) and (AST) activity whereas activity of ALP reduced significantly (P<0.05). The results showed significant reduction in the antioxidant enzyme activity and increases in (MDA). The mean bone matrix mineralization and intracellular calcium content of the MSCs also reduced significantly (P<0.05).

Conclusions: Oral consumption of cadmium affects osteogenic differentiation potential of MSCs via membrane damage, reduction of calcium deposition and metabolic changes. Thus, it might be considered as a probable factor involve in cadmium related osteoporosis.