Abstract

  Organic hydroperoxides such as t-butyl hydroperoxide and cumene hydroperoxide have been implicated to cause oxidative stress leading to damage in membrane lipids, proteins, carbohydrates and DNA. This study was aimed to develop an in vivo animal model. The effects of hydroperoxides on testicular tissue and epididymal sperm were investigated. Male Wistar rats aged 10 - 12 weeks were randomly placed in groups and received standard rat chow and water ad libitum. Animals were injected intraperitoneally with saline (0.5 ml), t-butyl hydroperoxide (5, 10, 20 and 40 µM; 0.5 ml) or cumene hydroperoxide cHP (2.5, 5, 10 and 20 µM; 0.5 ml) over a 60 day period. It was found that cumene hydroperoxide cHP (10 and 20 µM) and t-butyl hydroperoxide tbHP (20 and 40 µM) led to significantly lower epididymal sperm concentrations and motility. Superoxide dismutase and glutathione activities were also higher with an accompanying increase in lipid peroxidation in both testicular tissue and epididymal sperm. It can be concluded thatin vivo intraperitoneal administration of organic hydroperoxides negatively affect the male reproductive system. We have therefore successfully created an animal model to test the adverse effects of oxidative stress on male reproductive parameters, thereby, enabling us to study possible in vivo treatments.   Key words: Hydroperoxide, sperm, motility, lipid peroxidation, superoxide dismutase, glutathione.

Highlights

  • Many environmental, physiological and genetic factors have been implicated in poor sperm function and infertility (Kovacic and Jacintho, 2001)

  • A significantly (p < 0.001) lower epididymal sperm concentration was observed in animals injected with 10 μM (67.00 ± 5.73 x 106/ml) and 20 μM (58.67 ± 4.80 x 106/ml) of cumene hydroperoxide (cHP) and 20 μM (65.50 ± 4.05 x 106/ml) and 40 μM (59.17 ± 4.10 x 106/ml) of t-butyl hydroperoxide (tbHP) when compared to the control group (109 ± 10.88 x 106/ml) (Table 1)

  • Sperm from animals injected with cHP (10 μM: 26 ± 4.30%; 20 μM: 18 ± 4.63%) and tbHP (20 μM: 20 ± 5.24%; 40 μM: 17 ± 3.39%) showed a significant (p < 0.001) lower motility when compared to sperm from control animals (66.60 ± 3.36%) (Figures 1A and B)

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Summary

Introduction

Physiological and genetic factors have been implicated in poor sperm function and infertility (Kovacic and Jacintho, 2001). Free radical-induced oxidative damage to sperm is one such condition and it is gaining considerable attention due to its contribution to sperm damage (Agarwal et al, 2003). A better understanding of how these conditions affect sperm. OS is a cellular condition associated with an imbalance between the production of free radicals, mainly reactive oxygen species (ROS) and their scavenging capacity by antioxidants. When the production of ROS exceeds the available antioxidant defence, significant oxidative damage occurs to many cellular organelles due to damage to lipids, proteins, DNA and carbohydrates. These processes can lead to cell death. Sperm is susceptible to oxidative damage due to its unique structural composition of high polyunsaturated fatty acid content in its plasma membrane (Garg et al, 2000; Lenzi et al, 2000; Sanocka and Kurpisz, 2004)

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