Spermatogenesis is an extremely active replicative process capable of generating approxi mately 1,000 sperm a second. The high rates of cell division inherent in this process imply correspondingly high rates of mitochondrial oxygen consumption by the germinal epithelium. However, the poor vascularization of the testes means that oxygen tensions in this tissue are low1 and that competition for this vital element within the testes is extremely intense. Since both spermatogenesis2 and Leydig cell steroidogenesis3,4 are vulnerable to oxidative stress, the low oxygen tension that characterizes this tissue may be an important component of the mechanisms by which the testes protects itself from free radical-mediated damage. In addition, the testes contain an elaborate array of antioxidant enzymes and free radical scavengers to ensure that the twin spermatogenic and steroidogenic functions of this organ are not impacted by oxidative stress. These antioxidant defence systems are of major importance because peroxidative damage is currently regarded as the single most important cause of impaired testicular function underpinning the pathological consequences of a wide range of conditions from testicular torsion to diabetes and xenobiotic exposure. This chapter sets out the specific nature of these antioxidant defence systems and also reviews the factors that have been found to impair their activity, precipitating a state of oxidative stress in the testes and impairing the latter’s ability to produce viable spermatozoa capable of initiating and supporting embryonic development.

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Antioxidant systems and oxidative stress in the testes.

Cyclophosphamide (CP) as an anticancer alkylating agent has been known as a male reproductive tract toxicant. The aim of this study was to examine whether Satureja khuzestanica essential oil (SKEO) as an established herbal antioxidant, might protect tract rat reproductive system from toxicity of CP. To reach this aim, total antioxidant power (TAP) and lipid peroxidation (LPO) in testis and plasma, blood levels of sex hormones, sperm characteristics, DNA integrity and chromatin quality, and fertility in male rats were tested. Histopathological analysis of testes and epididymides and staining of mast cells were performed for assessment of spermatogenic disorders. CP (6 mg/kg/day) and SKEO (225 mg/kg/day) were administered alone or in combination by gavage for 28 days. In the CP-exposed rats, testicular and plasma LPO increased, TAP decreased, plasma testosterone diminished, and both spermatogenesis and fertility were impaired. In CP-treated rats, a decrease in sperm quality was associated with increased DNA damage and decreased chromatin quality. Coadministration of SKEO significantly improved CP-induced changes in plasma testosterone, sperm quality, spermatogenesis and fertility, toxic stress, and DNA damage. It is concluded that CP-induced toxic effects on androgenesis and spermatogenesis is mediated by free radicals. SKEO protects reproductive system from toxicity of CP through its antioxidant potential and androgenic activity.

Protection of cyclophosphamide-induced toxicity in reproductive tract histology, sperm characteristics, and DNA damage by an herbal source; evidence for role of free-radical toxic stress.

Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats.

http://ntur.lib.ntu.edu.tw/bitstream/246246/163202/1/07.pdf

Cyclophosphamide treatment causes impairment of sperm and its fertilizing ability in mice.

https://www.fertstert.org/article/S0015-0282(08)03281-0/pdf

Potential chemoprotective effect of melatonin in cyclophosphamide- and cisplatin-induced testicular damage in rats.

The present work examined the changes in testicular activities in relation to testicular oxidative stress in cyclophosphamide as well as human chorionic gonadotrophin (hCG) co-treated cyclophosphamide treated Wistar strain rats. Testicular activities were evaluated by the quantification of spermatogenesis and by the measurement of steroidogenic key enzyme activities along with plasma levels of testosterone. Testicular oxidative stress in relation to cyclophosphamide treatment was monitored by the study of products of free radicals like conjugated dienes and malondialdehyde (MDA) as well as the activity of testicular antioxidant enzymes like peroxidase and catalase. Cyclophosphamide treatment at the dose of 5 mg/kg body weight/day for 28 days resulted a significant diminution in the activities of testicular Δ5, 3β-hydroxysteroid dehydrogenase (Δ5, 3β-HSD), 17β-hydroxysteroid dehydrogenase (17β-HSD) activities, plasma level of testosterone along with significant reduction in the number of germ cells...

M. Mallick

Papers

Testicular gametogenic and steroidogenic activities in cyclophosphamide treated rat: a correlative study with testicular oxidative stress.