Abstract

Many recent studies have demonstrated that most nanoparticles (NPs) have an adverse or toxic action on male germ cells. In present study, protective effect of quercetin (Que) on titanium dioxide nanoparticle (NTiO2)-induced spermatogenesis defects in mice was investigated. Thirty-two Naval Medical Research Institute (NMRI) mice were randomly divided into four groups. Que group received 75mg/kg of Que for 42days. NTiO2 group received 300mg/kg NTiO2 for 35days. NTiO2 + Que group initially received 75mg/kg Que for 7days and was followed by concomitant administration of 300mg/kg NTiO2 for 35days. Control group received only normal saline for 42days. Sperm parameters, testosterone concentration, histological criteria, and apoptotic index were assessed. Product of lipid peroxidation (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were also evaluated for oxidative stress in testicular tissue. Administration of NTiO2 significantly induced histological changes in testicular tissue; increased apoptotic index; and decreased testicular weight, testosterone concentration, and sperm quality (p<0.01). In the testis, NTiO2 increased oxidative stress through an increase in lipid peroxidation and a decrease in SOD and CAT activities (p<0.05). Que pretreatment could significantly attenuate testicular weight; apoptotic index; and histological criteria including vacuolization, detachment, and sloughing of germ cells in seminiferous tubules. Serum and tissue testosterone levels were significantly increased in Que-pretreated mice (p<0.01). Sperm parameters including sperm number, motility, and percentage of abnormality were also effectively improved by Que pretreatment (p<0.01). Pretreatment of Que significantly ameliorated oxidative stress and increased the activities of SOD and CAT in testicular tissue. These results indicate that sperm production can be increased by Que pretreatment in NTiO2-intoxicated mice. The improved sperm quality and reverse testis histology by Que pretreatment may be a consequence of elevation testosterone concentration, reduction in germ cell apoptosis, and suppression of oxidative stress in testicular tissue.

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