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Metabolism Of 4‐Hydroxynonenal In Rat Organs In Response To Ethanol Feeding

4‐Hydroxynonenal (HNE) is one of the most abundant lipid peroxidation products and is highly reactive unsaturated aldehyde. The deleterious effects of HNE are ascribed to its post modification of many macromolecules, such as proteins, DNA, and phospholipid. HNE level is not only related to oxidative stress but also depends on the disposal rate via metabolism. Alcohol is known to induce oxidative stress and redox change both of which could potentially influence HNE level. In the present work, we investigated HNE level, redox change, and oxidative stress in various organs including plasma after rats were fed with alcohol for two weeks. Mitochondrial and cytosolic redox was estimated by measuring the ratios of 3‐hydroxybutyrate/acetoacetate (BHB/AcAc) and lactate/pyruvate (LAC/PYR), respectively. Alcohol induced redox shift to reductive state in most organs except kidney. Many oxidative stress biomarkers, such as ophthamate and 2‐hydroxybutyrate, were significantly increased in all organs including plasma after alcohol feeding. HNE and 4‐oxononenal (ONE) were elevated in most organs except brain and plasma. HNE‐glutathione (HNE‐GSH) conjugate was increased by alcohol in brain and kidney, but slightly decreased in liver and heart compared to control pair‐fed. Our data suggested that: (i) alcohol altered redox status in most organs but not in kidney; (ii) redox change is not the only factor causing oxidative stress; (iii) metabolic disposal of HNE is organ dependent.