Abstract
An experiment was conducted to study the response of rat tissues to low level exposure of arsenic (III) for different time periods. Rats were exposed to 0 (Gr. I, healthy control, n = 18) or 10 ppm arsenic (Gr. II, positive control, n = 18) through drinking water ad lib for a maximum period of 12 weeks. Six rats were sacrificed from each group under light chloroform anesthesia at the end of 4, 8 and 12 weeks of arsenic exposure for collection of blood, liver and kidneys. Samples were processed for estimation of oxidative stress indices and biochemical variables indicative of hepatic and renal functions. Tissue arsenic burden was measured at the end of 12 weeks of exposure. Arsenic treated rats (Gr. II) had comparatively poor body weight gain over time, and the mean body weights of these rats were significantly ( P < 0.05) lower from 10th weeks onwards. Oral exposure to arsenic for a period of 12 weeks significantly ( P < 0.05) increased arsenic burden in blood, liver and kidney from arsenic treated rats. This was associated with exposure duration-dependent rise ( P < 0.05) in lipid peroxidation in these tissues. Superoxide dismutase (SOD) and catalase (CAT) activities increased initially ( P < 0.05) in all the tissues followed by a declining trend and at the end of 12 weeks, the activities were non-significantly ( P > 0.05) lower than respective controls. Alterations in most of the biochemical parameters did not reach statistical significance ( P > 0.05). It was concluded from the present study that low dose arsenic exposure for a shorter period caused activation of intrinsic antioxidant defense whereas a prolonged insult suppressed it. However, biochemical parameters indicative of hepatic and renal dysfunction remained well within the normal range.
Published Version
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