Aim. To study the levels of nitric oxide (II) metabolites, lactate, endogenic carnitine and mitochondrial oxidoreductase activity in epididymis tissue at nitric oxide low synthesis and, based on the obtained data, to assess the functional condition of rat epididymis mitochondria.
Methods. 16 Wistar rats were allocated to two equal groups: The first group was administered L-NG-nitroarginine methyl ester (L-NAME), which is non-selective NO-synthase inhibitor, at a dose of 25 mg/kg for 7 days. The second group (the control group) got 0.9% sodium chloride solution administered as intraperitoneal injection for 7 days. Homogenate was obtained from epididymis tissue (head and tail), and mitochondria were isolated from it by differential centrifugation. Activities of mitochondrial enzymes (lactate dehydrogenase, succinate dehydrogenase and superoxide dismutase) were measured, as well as concentrations of NO metabolites, lactate, total protein and endogenous carnitine.
Results. Activity of succinate dehydrogenase was significantly decreased by 55 and 68%, lactate dehydrogenase activity - by 78 and 92%, superoxide dismutase - by 16 and 43% in the mitochondria of epididymis head and tail tissue, respectively in the group receiving 25 mg/kg of L-NAME, compared to the control group. The concentrations of NO metabolites decreased by 18 and 30%, lactate levels increased by 43 and 35%, the share of bounded carnitine decreased by 25% in epididymis tail. Changes of carnitine concentrations in epididymis head were non-significant.
Conclusion. In L-NAME-induced deficiency of NO in epididymis tissues mitochondria, statistically significant decrease in the activity of mitochondrial oxidoreductases and lactate accumulation was noticed, indicating the development of secondary mitochondrial dysfunction.
Nitric oxide-independent, thiol-associated ADP-ribosylation inactivates aldehyde dehydrogenase.