The possible protective effect of vitamin C on the kidney cortex of adult female albino rat after chronic exposure to malathion: a light and electron microscopic study

Background Chronic exposure to malathion is still a major medical problem in occupational and environmental settings. The raised issue of the antioxidants effect on different tissues provides a new line of protection against the inevitable exposure to insecticide residues in food or through environmental contamination. Aim The aim of the study was to determine the effects of vitamin C supplementation on renal cortical tissue after chronic exposure to malathion. Materials and methods Thirty female albino rats aged 3 months were divided into three equal groups: group I control adults were fed the basal diet; group II was given commercial malathion dissolved in distilled water orally by intragastric tube at a dose of 100 mg/kg/day for 2 months; and group III was given malathion in the previously described way at the same dose in addition to vitamin C (pure ascorbic acid powder) dissolved in distilled water and given orally by intragastric tube at a dose of 20 mg/100 g/day for 2 months. The specimens were obtained from the kidney and prepared for light and electron microscopic examinations. Morphometric and statistical studies were carried out in the three studied groups. Results It was observed that treatment with malathion disrupted the normal histological structure of the renal cortex. Thickened glomerular basement membrane was evident. There was widespread vacuolation of tubular lining epithelium and increased heterochromatin clumps in most of the nuclei. The mitochondria appeared disorganized with loss of cristae. The diameter of renal corpuscles and renal tubules increased, whereas tubular epithelium height decreased significantly compared with the control. Moderate improvement in the previous findings was detected on concomitant supplementation of vitamin C. Conclusion Vitamin C supplementation played a protective role on the renal cortex exposed to chronic malathion toxicity at the subcellular level.