Short-term levosimendan treatment protects rat testes against oxidative stress

M.B. Yuksel,I. Gecit,S. Kavak,H. Basel,H.A. Gümrükçüoğlu,H. Demir,İ. Meral

doi:10.1590/s0100-879x2012007500075

Abstract

The objective of this study was to evaluate the effect of short-term levosimendan exposure on oxidant/antioxidant status and trace element levels in the testes of rats under physiological conditions. Twenty male Wistar albino rats were randomly divided into two groups of 10 animals each. Group 1 was not exposed to levosimendan and served as control. Levosimendan (12 µg/kg) diluted in 10 mL 0.9% NaCl was administered intraperitoneally to group 2. Animals of both groups were sacrificed after 3 days and their testes were harvested for the determination of changes in tissue oxidant/antioxidant status and trace element levels. Tissue malondialdehyde (MDA) was significantly lower in the levosimendan group (P < 0.001) than in the untreated control group and superoxide dismutase and glutathione peroxidase (GSH-Px) levels were significantly higher in the levosimendan group (P < 0.001). Carbonic anhydrase, catalase and GSH levels were not significantly different from controls. Mg and Zn levels of testes were significantly higher (P < 0.001) and Co, Pb, Cd, Mn, and Cu were significantly lower (P < 0.001) in group 2 compared to group 1. Fe levels were similar for the two groups (P = 0.94). These results suggest that 3-day exposure to levosimendan induced a significant decrease in tissue MDA level, which is a lipid peroxidation product and an indicator of oxidative stress, and a significant increase in the activity of an important number of the enzymes that protect against oxidative stress in rat testes.

Highlights

Oxidative stress triggers a cascade that leads to the production of reactive oxygen species (ROS), accumulation of lipid peroxidation products such as malondialdehyde (MDA), massive secretion of systemic inflammatory mediators that can result in the development of systemic inflammatory response syndromes, impaired cell function, and multiple organ dysfunctions [1,2,3,4], while the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) play important roles in cell defense against oxidative stress
SOD, a family of enzymes that catalyze the dismutation of two superoxide anions (O2-·) to hydrogen peroxide (H2O2) and molecular oxygen, reduce tissue concentrations of superoxide radicals in order to prevent the induction of oxidative damage to lipids, proteins and DNA [23,24]
The elimination of H2O2 is effected by catalase or glutathione peroxidase, with the latter predominating in the case of the testes [25,26]

Summary

Introduction

Oxidative stress triggers a cascade that leads to the production of reactive oxygen species (ROS), accumulation of lipid peroxidation products such as malondialdehyde (MDA), massive secretion of systemic inflammatory mediators that can result in the development of systemic inflammatory response syndromes, impaired cell function, and multiple organ dysfunctions [1,2,3,4], while the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) play important roles in cell defense against oxidative stress. The high rates of cell division inherent in this process imply correspondingly high rates of mitochondrial oxygen consumption by the germinal epithelium The competition for this element within the testes is extremely intense. Despite the low oxygen tensions that characterize the testicular microenvironment, this tissue remains vulnerable to oxidative stress due to the abundance of highly unsaturated fatty acids and the presence of potential ROS-producing systems. Since both spermatogenesis and Leydig cell steroidogenesis are vulnerable to oxidative stress, the low oxygen tension may be an important component of the Received December 23, 2011.

Objectives

Methods

Findings

Conclusion