Abstract

Arsenic, a sulfhydryl reactive metalloid, found primarily in two forms: arsenite and arsenate, causing several human health problems, is considered as a dreaded agent against public health. It mainly spreads through groundwater contamination and affects human mainly through drinking water. Arsenic contaminated groundwater is now a major threat in some parts of India (the river basin of Ganga and Brahmaputra) and Bangladesh. The current authors belong to the region where arsenic poisoning and its consequences are spreading in an uncontrolled way. We are helpless to stop the spreading of geogenic groundwater arsenic contamination at present. Although most of the research on arsenic removal from drinking water and on toxicity profile has been carried out, very few preventive measures have been reported till date to balance the arsenic-induced cellular energy deficiency and oxidative stress-mediated cell death and cellular senescence. And, therefore, we need to think about alternative remedial to address such problems, which propel us to propose the current hypothesis that the adverse effects of energy imbalance due to arsenic toxicity in cells could be dodged by intake of moderate amount of alcohol. While pyruvate dehydrogenase complex is blocked by arsenic, glucose cannot be utilized through Kreb's cycle. However, alcohol can produce energy by bypassing the aerobic adenosine triphosphate (ATP) production machinery. In addition, arsenic poisoning incurs cellular oxidative stress which needs to be scavenged further. So to meet this secondary problem, we also suggest consuming red grape juice (a potent antioxidant and cytoprotective agent) in addition to alcohol (as per International Center for Alcohol Policies (ICAP) Drinking Guidelines) in our second part of the hypothesis. In conclusion, it can be suggested that the red wine which contains moderate amount of alcohol and high levels of red grape polyphenols, galic acid, resveratrol, and other antioxidants could be the best alternative to tackle the arsenic-induced cellular aging, senescence, and death.

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