Retracted: Is immunosuppression, induced by neonatal thymectomy, compatible with poor reproductive performance in adult male rats?

Abstract

With increasing knowledge that the immune system has a major impact on reproductive ‎health, the potential for cells arising in organs such as the thymus to alleviate oxidative stress ‎has been revealed. This study addresses the impact of neonatal thymectomy on male ‎reproductive function in pubertal and adult animals. Neonatal Sprague Dawley rats were allotted to four treatments consisting of fully thymectomized, partially thymectomized, intact, and sham-operated rats. Half of the rats in each treatment were sacrificed at 40 and the other half at 80 days of age. Testicular volume, ventral prostate and spleen weight, several sperm attributes (concentration, motility, livability, membrane integrity, sperm penetration into mucus, total antioxidant capacity, mitochondrial dehydrogenase activity), plasma superoxide dismutase, glutathione, and testosterone level as well as fertility decreased in thymectomized rats. Adrenal gland weight, sperm malondialdehyde level, indices of oxidative stress, sperm abnormality, testicular and sperm lipid peroxidation, protein carbonylation, and sperm reactive oxygen species generation increased in thymectomized rats. In thymectomized rats, the testes contained high levels of malondialdehyde but low levels of glutathione and ferric-reducing antioxidant power. Epididymal sperm reactive oxygen species, blood lipid peroxidation, and oxidative stress indices ‎‎in blood and spermatozoa were highest in fully thymectomized, intermediate ‎in partially thymectomized, and lowest in both pubertal and mature control rats. Blood levels of superoxide dismutase, lipid peroxidation indices, and ‎testosterone, and mitochondrial adenosine triphosphate and ‎dehydrogenase activities in epididymal spermatozoa were lowest in fully thymectomized, ‎intermediate in partially thymectomized, and highest in both pubertal and mature control rats.‎ The data indicated that increased oxidative stress and mitochondrial dysfunction might play a role in the mechanism of immunosuppression-induced testicular and sperm abnormalities.

Spermatotoxic Effects of Single-Walled and Multi-Walled Carbon Nanotubes on Male Mice

“…Sperm abnormality and viability were measured in duplicate (200 sperm per sample) after eosin-nigrosin staining (20,31). Spermatozoa with protoplasmic droplets, ab-axial tails, malformed heads, double tails, coiled tails, bent tails, and without tail or head were recorded as abnormal under a phase-contrast microscope (Olympus BX41; Olympus Optical Co. Ltd, Japan) (28,57).…”

“…Oxidative stress (OS), mitochondrial impairment, and their subsequent complications seem to play crucial roles in the xenobiotics-induced reprotoxicity and consequent infertility (20,21,(24)(25)(26)(27)(28)(29)(30). High sensitivity to OS, excessive reactive oxygen species (ROS) levels, and thiobarbituric acid reactive substances (TBARS) content could dramatically affect the functions of the reproductive organs (20,21,(26)(27)(28)(29)(30)(31)(32)(33)(34). For instance, oxidative injury and DNA damage studies indicated that high doses of MWCNT could cause DNA damage in murine sperm (35).…”

“…Cellular energy metabolism is pivotal in sperm forward motility (24,25,51), and there is ample evidence showing that xenobiotics could alter mitochondrial functionality and induce severe OS in different reproductive tissues (20,21,(27)(28)(29)(30). In this regard, Xu et al (52) reported that MWCNT caused severe damages to mitochondrial DNA in spermatocytes.…”

Can Melissa officinalis improve chromatin structure and sperm parameters in a rat model of varicocele?

“…Varicocelised rats in MO treatment and placebo groups were gavaged daily with 150 mg/kg of MO or normal saline for 10 weeks (a complete spermatogenesis cycle of rat) (Ommati et al., ) orally following operation.…”

Zingiber officinale mitigates diazinon-induced testicular toxicity via suppression of oxidative stress and apoptosis in mice model

“…Pathogenesis of tissue damage following DZN exposure is usually being attributed to oxidative injury [11]. Increasing oxidative stress through mitochondrial dysfunction and immunosuppression can lead to testicular injury and sperm abnormalities [12]. DZN with oxidative stress and generation of free radicals and increment of lipid peroxidation induce DNA fragmentation and apoptosis [5].…”