Abstract
Abstract
Background
Even though the widespread of nanoalumina and their benefits in all fields, its potential impacts on male reproductive system have limited information.
Objective
The present study was conducted to investigate the testicular dysfunction of nanoalumina and the protective role of pumpkin seed oil (PSO) against potential adverse impacts induced by alumina nanoparticles (Al2O3-NPs) in male rat.
Methodology
Al2O3-NPs were administered to the rat orally at a dose of 70 mg/kg body weight once a day for 28 successive days, while pumpkin seed oil was administered to the rat orally at 4 mL/kg b w before administration of Al2O3-NPs, once a day for 28 successive days. After the administration period, sperm concentration, motility, morphology, and DNA damage, as biomarkers of reproductive toxic effects, were evaluated using sperm analysis and comet assays, and histopathological examination of testis was performed. In addition, level of the serum testosterone hormones were estimated, and the levels of oxidative stress biomarkers that take part in the reproductive pathologies such as catalase, glutathione, and malondialdehyde were estimated.
Results
The present results revealed that Al2O3-NPs induced DNA damage in testicular cells, marked histopathological alterations, and caused a significant elevation in MDA in testicular tissue. There was a significant decline in GSH and CAT activities. Furthermore, there was a significant decline in serum testosterone level in the testicular tissue of Al2O3-NP-administered rats. In contrast, pumpkin seed oil co-administration alleviated DNA damage and improved the histopathological alterations in the testicular tissues. Moreover, pumpkin seed oil co-administration significantly reduced MDA and improved the antioxidant defenses in testicular tissue.
Conclusion
The current study concluded that Al2O3-NPs caused testicular dysfunction by generating oxidative injury. Otherwise, PSO co-administration successfully attenuated the adverse impacts of Al2O3-NPs via suppression of oxidative stress and apoptosis as well as enhancement of the antioxidant defense system.
Publisher
Springer Science and Business Media LLC
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