Assessment of blood and urine total antioxidant and oxidative status in alcohol and acetone fatal poisonings

Abstract

Abstract Heavy alcohol consumption is a common cause of fatal poisoning, unlike acetone poisoning, which is very rare. Although oxidative stress plays a crucial role in alcohol and acetone toxicity, no studies compare the total redox status in fatally poisoned individuals. The total antioxidant capacity (TAC), total oxidative status (TOS), and oxidative stress index (OSI) were examined in the blood and urine of patients fatally poisoned with ethanol (n = 21) and acetone (n = 21), along with healthy controls (n = 21). The TAC, TOS, and OSI concentrations were determined by means of colorimetric methods, and the statistical analysis was conducted through non-parametric tests. The blood TAC and TOS were significantly increased in the ethanol- and acetone-intoxicated cadavers as compared to the controls. The blood TAC levels above 55.12 nmol/mg of protein differentiate alcohol- and acetone-intoxicated subjects from the control group with a high sensitivity and specificity. The blood TAC was also positively correlated with the alcohol (r = 0.504), acetone (r = 0.476), and isopropanol blood levels (r = 0.514). However, the TAC, TOS, and OSI in the blood were poorly correlated with the corresponding urine concentrations. The urinary TAC in the ethanol-poisoned subjects was effectively enhanced in comparison to the control and acetone-poisoned subjects. The urinary TAC was also positively associated with the urine alcohol concentration (r = 0.413) and negatively correlated with the acetone (r = − 0.453) and isopropanol urine levels (r = − 0.36). Fatal alcohol and acetone intoxications disrupt the circulating redox status, favoring antioxidant reactions. Differences in the blood and urine redox homeostasis may be due to the organ toxicity of alcohol and acetone.