Dietary selenium fortification: a potential solution to chronic arsenic toxicity

Abstract

Selenium (Se), an important micronutrient and antioxidant, also acts as an antagonist of arsenic (As). Se supplementation of diet was investigated in mitigating chronic As toxicity in mammals. Experiments were conducted to determine whether Se supplementation in As-exposed rats might (i) decrease As-induced lipid peroxidation in liver, (ii) increase blood antioxidant status, and (iii) reverse suppression of the secondary antibody response. Male Wistar rats were exposed to As (40 and 80 ppm) in drinking water and received challenge diets with three different levels of Se (deficient: <0.01 ppm, adequate: 0.15 ppm, and fortified: 0.6 ppm) for 16 weeks. Clinical variables including behavior, body weight, and food and water consumption were recorded weekly, and blood sample was collected monthly. Antioxidant status was assessed through glutathione sulfhydryl (GSH) levels in whole blood. Lipid peroxidation in the liver was evaluated using the malondialdehyde (MDA) assay. The antibody response was measured using keyhole limpet hemocyanin as an immunogen. Se deficiency significantly increased hepatic lipid peroxidation and suppressed antibody production relative to the Se-adequate and -fortified groups, confirming that Se deficiency exacerbates the damage produced by As exposure. Se fortification markedly elevated the blood GSH level in both As-exposed groups, indicating protective effects. At adequate Se levels, rats showed signs of counteracting As-mediated toxicity. However, Se fortification produced more pronounced benefits against As-induced toxicity, a pattern that was particularly notable in the 40 ppm As group.

Keywords:

• mitigating arsenic toxicity
• arsenicosis
• dietary selenium
• selenium–arsenic interaction
• selenium antagonism of arsenic

Acknowledgments

This study was performed at the University of Calgary with a generous, multi-year grant provided by the Saskatchewan Pulse Development Board (JS) with matching support from the Natural Sciences and Engineering Research Council of Canada (JS). The authors warmly thank Luis Cruz and Sukhbir Nain for their pleasant and valuable help with various aspects of this study.