Quercetin mediated attenuation of cadmium‐induced oxidative toxicity and apoptosis of spermatogenic cells in caprine testes in vitro

Abstract

Cadmium (Cd), an environmental toxic heavy metal, has been reported to cause testicular toxicity, which contributes to the recent decline in male fertility worldwide. Quercetin (Qcn), a major dietary antioxidant, has been shown to have protective effects under various pathological conditions. However, whether Qcn provides protection against Cd‐stimulated testicular toxicity remains obscured. The present study was therefore aimed at investigating the ameliorative effect of Qcn supplementation on Cd‐induced toxicity in the goat testis in vitro in a dose‐(10, 50, and 100 μM) and time‐dependent (4 and 8 h) manner. Different cytotoxicity, genotoxicity, and biochemical analyses have been carried out using appropriate methods. Cytotoxicity in testicular cells induced by Cd treatment was apparently mitigated by Qcn treatment, evidenced by decreased apoptotic attributes or frequency in Qcn plus Cd‐treated groups compared to the only Cd‐treated groups. Qcn treatment provides substantial protection to the Cd‐triggered aggression in oxidative (increased MDA levels) and total antioxidant capacity (reduced FRAP activity) in testicular tissue, indicating the anti‐oxidative function of Qcn against Cd exposure. Moreover, Cd‐induced decline in antioxidant status (CAT, SOD, and GST activity) was markedly restored by Qcn supplementation in testicular tissue. In conclusion, this study shows that Qcn treatment significantly attenuated the Cd‐evoked testicular damage, suggesting its beneficial potential in preventing or at least in managing the gonadotoxicity in males induced by steadily increasing Cd contamination in the environment.

Thymoquinone induces apoptosis in temozolomide‐resistant glioblastoma cells via the p38 mitogen‐activated protein kinase signaling pathway

“…TQ is found to induce apoptosis, and this phenomenon might be responsible for its genotoxicity (DNA fragmentation assessed by TUNEL and DAPI). 29 , 30 , 31 , 32 TUNEL‐DAPI staining confirmed that TQ alone and TQ combined with TMZ caused apoptosis in xenograft tumors (Figure 5B ). Protein expression results were similar to those obtained in vitro with U251R cells.…”

“…Furthermore, MGMT expression was not significantly different between groups, hinting that neither TQ nor TMZ effectively alter MGMT expression in U251R cells. TQ is found to induce apoptosis, and this phenomenon might be responsible for its genotoxicity (DNA fragmentation assessed by TUNEL and DAPI) 29–32 . TUNEL‐DAPI staining confirmed that TQ alone and TQ combined with TMZ caused apoptosis in xenograft tumors (Figure 5B).…”

Protective effect of C‐phycocyanin and apo‐phycocyanin subunit on programmed necrosis ofGC‐1 spg cells induced byH2O2

“…In the process of germ cell development, a high level of ROS leads to a decrease in the quality and quantity of germ cells, and also affects the development of embryos. Bhardwaj et al found that oxidative damage of in germ cells could induce increased MDA and declined total antioxidant capacity, resulting in serious cell damage, and then lead to cell death through via activating necrosis or apoptosis 46,61 . Excessive ROS can have a negative impact on sperm quality, damaging cell membranes and nuclei, which can lead to decreased sperm quality and even death.…”

Selective inhibition of carbonic anhydrase IX by sulphonylated 1,2,3-triazole incorporated benzenesulphonamides capable of inducing apoptosis

“…The testicular cells/tissues were cultured in vitro in media-TCM199 and exposed to 10 µM concentration of given compounds for 6 h in a CO 2 incubator with 5% CO 2 and 95% humidity at 38 °C temperature. 22 , 23 …”