<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>13</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">P. V. Ingle</style></author><author><style face="normal" font="default" size="100%">S. M. Munot</style></author><author><style face="normal" font="default" size="100%">M. M. Thakare</style></author><author><style face="normal" font="default" size="100%">V. G. Kuchake</style></author><author><style face="normal" font="default" size="100%">S. J. Surana.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">“Alcohol vitamin A and Cancer” </style></title><secondary-title><style face="normal" font="default" size="100%">In Satellite Meeting of “Society for Free Radical Research - India (SFRR – India)” Organized by: Department of Biochemistry, theme based on “Free Radicals and Antioxidants in Human Health, Gene Regulation and Signal Transduction” held at All India Institu</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 Feb 11</style></date></pub-dates></dates><pub-location><style face="normal" font="default" size="100%">All India Institute of Medical Sciences (AIIMS) New Delhi. </style></pub-location><abstract><style face="normal" font="default" size="100%">Chronic and excessive alcohol intake is associated with an increased risk of a variety of cancers (e.g., oral cavity, larynx, esophagus, liver, lung, colorectal, and breast). Retinoids (vitamin A and its derivatives) are known to exert profound effects on cellular growth, cellular differentiation, and apoptosis, thereby controlling carcinogenesis. Lower hepatic vitamin A levels have been well documented in alcoholics. Substantial research has been done, investigating the mechanisms by which excessive alcohol interferes with retinoid metabolism. More specifically, alcohol acts as a competitive inhibitor of vitamin A oxidation to retinoic acid involving alcohol dehydrogenases and acetaldehyde dehydrogenases; alcohol-induced cytochrome P450 enzymes (CYP), particularly CYP2E1, enhance catabolism of vitamin A and retinoic acid; and alcohol alters retinoid homeostasis by increasing vitamin A mobilization from liver to extra hepatic tissues. As a consequence, long-term and excessive alcohol intake results in impaired status of retinoic acid, the most active derivative of vitamin A and a ligand for both retinoic acid receptors and retinoid X receptors. Moreover, this alcohol-impaired retinoic acid homeostasis interferes with retinoic acid signaling (e.g., down-regulates retinoid target gene expression) and retinoic acid “cross-talk” with the mitogen-activated protein kinase [(MAPK), including Jun N-terminal kinase, extracellular signal-regulated kinase, and p38 kinase] signaling pathway. In addition, restoration of retinoic acid homeostasis by retinoic acid supplementation restored the normal status of both retinoid and MAPK signaling, thereby maintaining normal cell proliferation and apoptosis in alcohol-fed animals. These observations would have implications for the prevention of alcohol-promoted liver (and peripheral tissue) carcinogenesis. However, a better understanding of the alcohol–retinoid interaction and the molecular mechanisms involved is needed before retinoids can be pursued in the prevention of alcohol-related carcinogenesis in human beings, particularly regarding the detrimental effects of polar metabolites of vitamin A. </style></abstract></record></records></xml>