Copper (Cu), one of the essential transition metal acts as a prosthetic group for variety of proteins and metalloenzymes. However, it may be hazardous when administered in excess. Copper induced memory impairment and progression of neurodegenerative diseases have not yet been fully elucidated. The aim of the present study was to investigate the effect of exposure to copper sulphate (10mg/kg and 20mg/kg body weight, daily for 16 weeks) on brain copper concentration, few biochemical parameters indicative of oxidative stress and on different neurobehavioral functions in male Sprague Dawley rats. Copper-administered animals showed significant increase in brain copper concentration and a depleted Ceruloplasmin level. Different neurobehavioral studies revealed impaired memory and motor coordination in copper exposed rat. Spontaneous locomotors activity and depression symptoms were also noted in copper intoxicated rats. 8-hydroxy-2' -deoxyguanosine (8-OHdG) level, one of the predominant forms of free radical-induced oxidative lesions, and has been widely used as a biomarker for oxidative stress, increased in copper treated group. Copper induced oxidative stress in the brain was also evident from the increased lipid per oxidation (LPO) and nitrite level, depletion of reduced glutathione (GSH), and reduced activities of the antioxidant enzymes such as superoxide dismutase (SOD), and catalase. The present study thus suggests a significant correlation between copper induced oxidative stress and changes in neurobehavioral function in rats. The changes were more pronounced in animals exposed to a higher dose of copper (20mg/kg) than the lower dose.

Arsenic (As) is naturally occurring toxic metalloid which is considered as a serious environmental and health concern. Red blood cells are the prime target for any toxicants as their population is higher in systemic circulation. High prevalence of anaemia too has been reported from arsenic contaminated area, suggesting possible linkage between arsenic and the damaging effects on RBCs. The exact mechanism for these effects is still not clear, however, oxidative/nitrosative stress might be one of the causative factors to play a key role. The present study was planned to evaluate the protective effects of a metal chelator, MiADMSA either alone or in combination with a natural antioxidant (gallic acid) for the reversal of arsenic induced oxidative damage in red blood cells. We collected rat RBCs and cultured them in appropriate medium. They were incubated with MiADMSA and gallic acid and then treated with sodium arsenite at 37 C. Hemolysates were prepared and assayed for various biochemical parameters such as oxidative/nitrosative variables, osmotic fragility, acetylcholinesterase activity, and cellular metal accumulation. We found there was reversibility of oxidative/nitrosative stress variables, elevated cellular antioxidant power, and decreased osmotic fragility of red blood cells both in MiADMSA alone as well as in combination with gallic acid treated group compared with arsenic treated group. In conclusion, MiADMSA efficiently participated in the reversal of arsenic induced oxidative/nitrosative damage in red blood cells where as Gallic acid improved its reversal when given in combination with MiADMSA.

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Background: Presently arsenicosis is considered as dangerous health issues including cancer. Urinary bladder is one of the common target organs for developing carcinogenesis by arsenic exposure due to accumulation of arsenic toxic metabolites in bladder. The mechanism involving urinary bladder carcinogenesis is still mysterious. Although there are multiple studies revealed about oxidative/nitosative stress, which plays main role for carcinogenesis, but no study evaluated the associated factor that linked with it as early sign to identify bladder carcinogenesis using a rat model. This study thus will be useful in predicting early sign for arsenic exposed urinary bladder carcinogenesis. Objective: We evaluated 8-Hydroxy-2-deoxyguanosine (8-OHdG) and Matrix Metalloproteinases-9 (MMP-9), which may be the possible associated factors along with oxidative/nitrosative stress as early sign for developing urinary bladder carcinogenesis upon arsenic and its metabolites exposure. Methods: Male Sprague Dawley rats were exposed to 25 ppm of sodium arsenite and its metabolite Dimethylarsinic Acid (DMA) via drinking water for a period of 16 weeks. The carcinogenic potentials were evaluated using various biochemical parameters indicative of oxidative/ nitrosative stress, ELISA of 8-OHdG as biomarker of oxidative/nitrosative stress induced DNA damage, which acts as a bridge between DNA damage and carcinogenesis. We also determined MMP-9 as potential pro-oncogenic biomarker associated with DNA damage. Results: High accumulation of arsenic was noted in tissues accompanied by a significant alteration of oxidative/nitrosative variables in liver and urinary bladder like significant changes in positive predictor of 8-OHdG and MMP-9 both in serum as well as urinary bladder tissue in animals exposed to arsenic and its metabolites. Conclusion: Early sign of urinary bladder carcinogenesis evaluated possibly by co-linking between oxidative/ nitrosative stress, 8-OHdG, MMP-9 and metal accumulation.