Disease relevance of ethanol

• Both the 1-hydroxyethyl and 2-hydroxyethyl radicals may play a role in ethanol-mediated toxicity [1].

Psychiatry related information on ethanol

• Transmitters for continuous biotelemetric recording of body temperature and motor activity were implanted i.p. in normal (N) adult rats, offspring of dams fed a liquid diet supplemented with ethanol (E), and pair-fed control offspring (P) [2].
• Rat ventral prostate xanthine oxidase bioactivation of ethanol to acetaldehyde and 1-hydroxyethyl free radicals: analysis of its potential role in heavy alcohol drinking tumor-promoting effects [3].

High impact information on ethanol

• Ethanol is converted to a free radical metabolite, the 1-hydroxyethyl radical in chemical reactions that generate hydroxyl radicals, in incubations of rat liver microsomes and in vivo [4].
• Pregnant rats were exposed to E vapors during days 7-18 of gestation, and we compared the responses of their 55- to 60-day-old offspring (E rats) to those of control (C) dams [5].
• CRF, but not VP hnRNA levels were also significantly higher in the PVN of shocked E offspring [5].
• Extensive ESR spin-trapping studies have shown that ethanol is oxidized to 1-hydroxyethyl radical (HER) by rat and deer mice liver microsomal systems [6].
• Ethanol can be oxidized to the 1-hydroxyethyl radical (HER) by rat and deer mice liver microsomal systems [7].

Biological context of ethanol

• Chim. Phys. 88, 967-976). the rate constant reaction of 1-hydroxyethyl free radicals with Cu,Zn-SOD was measured separately by competition kinetics with the spin trapping agent alpha-(4-pyridyl 1-oxide) N-terbutylnitrone (4-POBN), after having measured the rate constant of scavenging of 1-hydroxyethyl free radicals by 4-POBN in the absence of SOD [8].
• IL-1 also suppressed 24-h food consumption in N and P rats and water consumption in P rats, but it did not produce significant anorexia and adypsia in E rats [2].
• Cytochrome P450 reductase-mediated anaerobic biotransformation of ethanol to 1-hydroxyethyl-free radicals and acetaldehyde [9].
• These mechanisms include: oxidative stress and lipid peroxidation; immunogenic processes initiated by formation of protein adducts of acetaldehyde, other aldehydes and 1-hydroxyethyl radicals; and activation of Kupffer cells by endotoxin and subsequent cascade of events that involved cytokines, chemokines, and adhesion molecules [10].

Anatomical context of ethanol

• Recent studies from the laboratory reported the presence in highly purified liver nuclear preparations free of endoplasmic reticulum, mitochondria or cytosol, of an ethanol metabolizing group of enzymes (NEMS) leading to acetaldehyde and to hydroxyl and 1-hydroxyethyl (1HEt) free radicals [11].

Gene context of ethanol

• CYP2E1 is also very effective in generating reactive oxygen intermediates such as superoxide radical and H2O2, oxidizing ethanol to the 1-hydroxyethyl radical, and has a high NADPH oxidase activity [12].
• The sensitivity of PR determination on SMs and CBs was SM (SH) 71%, SM (ETH) 6.0%, CB (SH) 25%, CB (ETH) 33%, CB (FOR) 80% [13].
• The ESR signal intensity of the 1-hydroxyethyl radical increased with higher concentrations of phosphate [14].
• Interaction of 1-hydroxyethyl radical with antioxidant enzymes [15].
• IL-1 produced a marked increase in body temperature, which was significantly lower in E rats than in N and P rats [2].

Analytical, diagnostic and therapeutic context of ethanol

• Intravenous administration of the spin-trapping agent alpha-(4-pyridyl-1-oxide)-N-t-butylnitrone (POBN) to anesthetized but otherwise untreated rats was used to test for formation of 1-hydroxyethyl radicals in vivo [16].
• Taken together, these data indicate that 1-hydroxyethyl radicals are formed in vivo and can be readily detected in bile when high concentrations of POBN are achieved through intravenous injection [16].

References