Hypoxia-Like Effect of L-Arginine in Seminal Vesicle and Epididymis of Rats

Abstract

INTRODUCTION: The effect of L-arginine on metabolic processes is mediated by nitric oxide (II), whose pool is regulated by several enzymes. In the literature, the mutual influence of oxygen deficit and NO production is described. Besides, both processes can be regulated by exogenous L-arginine.
 AIM: To evaluate participation of L-arginine in the development of adaptive response to chronic normobaric hypoxia of tissues of reproductive system of male rats and to study its influence on metabolic changes in normoxia.
 MATERIALS AND METHODS: The experiment was conducted on Wistar stock rats (males, n = 8) which were divided to the following groups: (1) animals receiving L-arginine injections of 500 mg/kg of body weight for 10 days; (2) animals of control group receiving 0.9% NaCl solution; (3) animals subjected to chronic normobaric hypoxia in a hermetic chamber, observed once a day for 14 days until the oxygen concentration in the air decreased by 10%; (4) animals of the control group observed in a ventilated chamber; (5) animals subjected to hypoxia and injections of L-arginine. The material for analysis was the mitochondria and mitochondria-free fraction of the cytoplasm of the seminal vesicles, of the head and tail of the epididymis. The parameters were evaluated photometrically using diagnostic and enzyme immunoassay kits.
 RESULTS: The animals receiving L-arginine showed increase in the amount of -subunit of hypoxia-induced factor in the cytoplasm of seminal vesicles by 132% (p = 0.01), in the tail of epididymis by 32% (p = 0.02) and reduction in mitochondria by 45% (p = 0.01) and 60% (p = 0,002), respectively, a decrease in succinate levels by 40% (p = 0.005) and 51% (p = 0.0009), an increase in the concentration of lactic acid in the cytoplasm by 194% (p = 0.03) and 253% (p = 0.018), a decrease in cytochrome oxidase activity from 0.96 [0.66; 1.69] RU/mg of protein to 0.27 [0.23; 0.32] (p = 0.0009) and from 1.04 [0.84; 1.33] to 0.26 [0.14; 0.37] (p = 0.003), relative to the control group. The observed changes are characteristic of the state of hypoxia and are explained by the cell switching over to glycolytic pathway of energy production, in contrast to mitochondrial pathway in normoxia. The combined effect of hypoxia and arginine partially enhanced each other's effects.
 CONCLUSION: L-arginine causes hypoxia-like state in cells through activating -subunit by hypoxia-induced factor, reducing cytochrome oxidase activity, increasing glycolysis, and also partially enhances the effects of chronic normobaric hypoxia.