Adaptive Serum Biochemistry Responses to Ethanol Administration in a Mouse Model: Implications for Metabolic Regulation Under Analgesia

Analgesia, or reduced pain sensitivity, can result from pharmacological or stress-induced mechanisms, but human studies are limited by complex physiological and psychological variables. This study aimed to evaluate the impact of ethanol consumption on key metabolic markers in two genetically distinct mouse lines selectively bred for pain sensitivity: high analgesia (HA) and low analgesia (LA). Forty-eight male Swiss-Webster mice were randomly assigned to four groups: HA and LA with or without heavy alcohol (ethanol) exposure. Blood serum was analyzed for its lipid profile, enzymatic activity, electrolyte levels and regulatory/energetic compounds. In HA mice, ALAT and AspAT activities and, albumin, creatinine, iron, and potassium levels were elevated, whereas glucose and sodium levels were decreased. LA mice presented increased bilirubin, cholesterol, LDL, HDL, and lipase activity. ChE, LDH, and CK activities differed significantly between the HA and LA groups. Ethanol intake influenced potassium, magnesium, and sodium serum concentrations. Discriminant analysis highlighted distinct biochemical profiles depending on the LA and HA groups. HA mice predominantly exhibit cytolytic liver damage, altered muscle metabolism, and increased iron levels, indicating oxidative stress. HA and LA display distinct adaptive metabolic strategies: protein/muscle and lipid/electrolyte metabolism, respectively. Genetic differences between HA and LA mice determine different metabolic responses to ethanol.