Abstract
Autophagy is an important catabolic process for the clearance of damaged or superfluous proteins and organelles. The role of ethanol in the regulation of autophagy remains controversial, with some studies showing induction of autophagy by ethanol while others show inhibition. Nevertheless, the view that maintenance of adequate levels of autophagy protects against ethanol induced damage is widely supported. We investigated the role of zinc in the modulation of autophagic flux in human hepatoma cells VL‐17A. LC3II/LC3I ratio, p62 and Beclin‐1 expression and autophagosomes number were analyzed in cells incubated in medium containing 0, 10, 20 or 40µM of zinc with or without 100 mM of ethanol, in presence or absence of the autophagy inhibitor chloroquine. The effect on autophagic flux of co‐incubation with lipopolysaccharide was also investigated. Lastly, labile zinc was analyzed in cells exposed to ethanol and the autophagy inhibitor 3‐methyladenine. Excess zinc had an additive effect on the induction of autophagy by ethanol and lipopolysaccharide. In addition, 3‐methyladenine treatment decreased labile zinc in cells. Our results indicate that zinc is a positive regulator of autophagic flux and support the notion that zinc protective effects against ethanol induced damage are mediated by autophagy.Grant Funding Source: Supported by NIH 1R03AA022451‐01
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