Methane biogenesis during sodium azide-induced chemical hypoxia in rats

摘要

Previous studies demonstrated methane generation in aerobic cells. Our aims were to investigate the methanogenic features of sodium azide (NaNs)-induced chemical hypoxia in the whole animal and to study the effects of L-a-glycerylphosphorylcholine (GPC) on endogenous nethane production and inflammatory events as indicators of a NaNr elicited mitochondrial dysfunction. Group 1 of Sprague-Daw-lev rats served as the sham-operated control; in group 2, the animals were treated with NaN3 (14 mg-kg"1-day~1 sc) for 8 days. In group 3, the chronic NaN3 administration was supplemented with daily oral GPC treatment. Group 4 served as an oral antibiotic-treated control (rifaximin, 10 mg-kg-day) targeting the intestinal bacterial flora, while group 5 received this antibiotic in parallel with NaN3 treatment.