Protective effect of Petroselinum crispum methanolic extract against acrylamide-induced reproductive toxicity in male rats through NF-ĸB, kinesin, steroidogenesis pathways.

This study examined the protective effects of a Petroselinum crispum (P. crispum) methanolic extract on reproductive dysfunction induced by acrylamide in male rats. A total of 40 rats were divided into four groups (n=10). The control group received distilled water, the acrylamide group received 10 mg/kg of acrylamide, the P. crispum group received 100 mg/kg of P. crispum extract, and the combined group was pretreated with P. crispum for two weeks before co-administration of P. crispum and acrylamide. All administrations were administered orally using a gastric tube for eight weeks. Acrylamide decreased testosterone levels but did not affect levels of FSH or LH. It also increased testicular levels of (MDA) malondialdehyde and reduced activity of (SOD) superoxide dismutase and impairment of sperm parameters. Furthermore, the administration of acrylamide resulted in an elevation of tumor necrosis factor-alpha (TNF-α) levels and a reduction in the levels of steroidogenic acute regulatory protein (STAR) and cytochrome P450scc (P450scc). Acrylamide negatively affected the histopathological outcomes, Johnsen's score, the diameter of seminiferous tubules, and the thickness of the germinal epithelium. It also upregulated the expression of NF-ĸB P65 and downregulated the expression of kinesin motor protein. In contrast, treatment with P. crispum extract restored the levels of antioxidant enzymes, improved sperm parameters, and normalized the gene expression of TNF-α, IL-10, IL-6, iNOS, NF-ĸB, STAR, CYP17A1, 17ß-HSD and P450scc. It also recovered testicular histological parameters and immunoexpression of NF-ĸB P65 and kinesin altered by acrylamide. P. crispum showed protective effects against acrylamide-induced reproductive toxicity by suppressing oxidative damage and inflammatory pathways.

Ameliorative effect of Odontonema cuspidatum extract against testicular damage induced by sodium nitrite in rats.

Background: Sodium nitrite (NaNO2) is a chemical substance used to enhance taste, add color, and keep food products fit for consumption for a longer time. NaNO2 gives rise to a negative adverse effect on male reproductive function. Odontonema cuspidatum (OC) is a natural plant that possesses antioxidant capacity. Aim: Our research evaluates the potential beneficial effect of OC extract on the harmful effects caused by NaNO2 on the testicular tissue and sperm characteristics of male rats. Methods: Four groups with a total of forty rats: the control, the NaNO2-received group, the OC-administered group, and the fourth group received both NaNO2 and OC. All groups were administered daily for two months. Sperm characteristics, testicular antioxidant status, qRT-PCR, and histopathological changes were evaluated. Results: Coadministration of NaNO2 and OC, in comparison with NaNO2 alone, contributed to a notable enhancement in acrosomal integrity, decreasing sperm abnormalities and restoring serum testosterone levels. Moreover, such coadministration reduced the oxidative stress marker, malondialdehyde (MDA), and increased superoxide dismutase (SOD) in testicular tissue, lowering TNF-α gene expression, and increasing the expression of P450scc and StAR genes. In addition, the NaNO2 and OC combination decreased the testicular histopathological changes and the Caspase-3 and Proliferating cell nuclear antigen (PCNA) immunoexpression in seminiferous tubules compared with the NaNO2 group. Conclusion: The extract of OC exhibited the ability to decrease oxidative stress and ameliorate the detrimental effects caused by NaNO2.

Gamma-irradiation-induced testicular oxidative stress and apoptosis: Mitigation by l-carnitine.

The current study evaluated the potential ameliorative and protective impacts of l-carnitine (L-CAR) against γ-irradiation (RAD)-induced oxidative stress and apoptosis in mice testes. Male Swiss mice were allocated into four groups (n = 7). Group 1 served as a control that received saline intraperitoneally (IP). Group 2 received L-CAR (10 mg/kg bw/day; IP in saline) for 17 days. Group 3 received saline for 17 days and on day 7 exposed to RAD at a dose of 0.1 Gy per day for consecutive 10 days. Group 4 (L-CAR + RAD), received L-CAR same as in group 2 and on day 7 exposed to RAD for consecutive 10 days. Testicular antioxidants (malondialdehyde, MDA; γ-glutamyl-cysteine synthetase, gGCS; and catalase) were altered by γ-irradiation. Preadministration of L-CAR protected γ-irradiated mice from altered changes induced by γ-irradiation. γ-Irradiation affected the mRNA expression of pro-apoptotic, apoptotic, and anti-apoptotic genes (c-jun, c-fos, Bcl-xl, caspase-3, and BAX). All altered genes were ameliorated by prior l-carnitine administration to γ-irradiated mice. Testicular cells showed deformities and edema with congestion in seminiferous tubules and strong immunoreactivity for caspase-9 and a decrease in immunoreactivity of Bcl-2 in histological and immunohistochemical examination. Prior administration of L-CAR to γ-irradiated mice protected this group from reported changes in caspase-9 and Bcl-2 immunostaining. In conclusion, the current study provides evidence for the protective and ameliorative impacts of L-CAR against γ-irradiation-induced testicular oxidative stress and apoptosis at biochemical, molecular, and cellular levels.