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IL‐6 family members are sensitive to alcohol‐induced oxidant stress in rat plantaris muscles

Chronic alcohol abuse may produce oxidant stress and lead to muscle wasting and dysfunction. Our goals were to (1) minimize oxidant stress and attenuate plantaris atrophy by supplementing diets of alcohol‐fed rats with a glutathione (GSH) precursor, procysteine (PRO), and (2) identify the role of IL‐6 family members in alcoholic myopathy. After 35 weeks of daily alcohol ingestion, rats displayed plantaris atrophy, decreased GSH levels, decreased activities of GSH reductase and GSH peroxidase, and increased NADPH oxidase‐1 gene expression. Further, gene expressions of several catabolic factors were induced, including IL‐6, oncostatin M, atrogin‐1, and MuRF. Interestingly, 12 weeks of PRO supplementation in alcohol‐fed rats restored GSH levels and attenuated plantaris atrophy, but did not reduce other markers of oxidant stress or levels of these catabolic factors. Instead, PRO induced IGF‐1, and two anabolic IL‐6 family members, ciliary neurotrophic factor and cardiotrophin‐1. Together, these data suggest that PRO does not "turnoff" alcohol‐induced oxidant stress, but rather stimulates anabolic pathways to compete against these persistent catabolic factors. Supported by NIH/NIAAA (AA07190‐01A1) to JSO.