Bladder cancer is defined as a urinary tract malignancy that threatens men’s and women’s health. Due to the side effects of common chemotherapies, novel therapeutic strategies are necessary to overcome the issues concerning bladder cancer treatments. Nanotechnology has been suggested as a means to develop the next-generation objectives of cancer diagnosis and treatment among various novel therapies. Owing to the special characteristics that they can offer, silver nanoparticles (AgNPs) were investigated in this study to evaluate their apoptotic impact on bladder cancer 5637 cells. In this study, an MTT assay was conducted and appropriate concentrations of AgNPs were selected. Moreover, reactive oxygen species (ROS) production and apoptosis levels were determined using fluorimetric and Annexin/PI flow cytometry assays, respectively. Moreover, the activity of caspase 3,7, mRNA expression of Bax (Bcl-2-associated X) and Bcl-2 (B-cell lymphoma 2) were assessed based on colorimetric and qRT-PCR methods, respectively. The results indicated that AgNPs can significantly reduce the viability of 5637 cells in a dose-dependent mode as well as having the ability to elevate ROS production. Flow cytometry data showed that AgNPs lead to a remarkable increase in the apoptosis rate as compared with the control. Consistent with this, the induction of apoptosis was revealed by the overexpression of Bax, accompanied by a reduction in Bcl-2 expression compared to the control. Furthermore, AgNPs remarkably stimulated caspase 3,7 activation. In summary, AgNPs can mediate apoptosis in 5637 cells via excessive ROS formation, up-regulating Bax/Bcl-2 expression, and caspase 3,7 activation.

Some reports emphasize that zinc oxide nanoparticles (ZnO NPs) are detrimental to the reproductive organs of animals. As such, this research aimed at exploring the apoptotic potential of ZnO NPs on testis along with the beneficial role of Vitamins (V) A, C, and E against ZnO NP-induced damage. To this aim, a population of 54 healthy, male Wistar rats were used in this work and then assigned into nine groups of 6 rats as G1: Control 1 (Water); G2: Control 2 (Olive oil); G3: VA (1000 IU/kg), G4: VC (200 mg/kg), G5: VE (100 IU/kg), G6: ZnO NPs exposed animals (200 mg/kg); and G7, 8 and 9: ZnO NPs-exposed animals that were pre-treated with either VA, C, or E. Apoptosis rates were estimated by measuring the level of apoptotic regulatory markers including Bcl-2-associated X (Bax) and B-cell lymphoma protein 2 (Bcl-2) using western blotting and qRT-PCR assays. The data indicated that ZnO NPs exposure elevates the level of Bax protein and gene expression, whereas the protein and gene expression of Bcl-2 was reduced. Further, the activation of caspase-3,7 occurred after exposure to ZnO NPs, while the above alterations were significantly alleviated in the rats that were co-treated with VA, C, or E and ZnO NPs relative to the rats in the ZnO NPs group. In summary, VA, C, and E exerted anti-apoptotic functions in the testis of rats following administration of ZnO NPs.

The protective effects of vitamins E and D, stemming from their antioxidant and anti-inflammatory capabilities were investigated in the context of tamoxifen-induced liver toxicity. The study involved twenty-five female rats divided into five experimental groups: group C (olive oil: 500 L), group T (tamoxifen: 40 mg/kg), groups TE (tamoxifen: 40 mg/kg and vitamin E: 100 IU/kg), group TD (tamoxifen: 40 mg/kg and vitamin D: 500 IU/kg) and group TED (tamoxifen: 40 mg/kg, vitamin E: 100 IU/kg and vitamin D: 500 IU/kg). Calorimetric methods were used to measure biochemical variables, hepatic level of Total antioxidant capacity (TAC), Total oxidant status (TOS), Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx). Hepatic level of tumor necrosis factor- (TNF-) was assayed by ELISA.Hematoxylin-eosin staining method was also employed to assess Tamoxifen-induced liver lesions. Tamoxifen treatment resulted in a significant increase in ALP (p-value<0.01), TOS, and OSI (p-value<0.01), a marked decrease in TAC level (p-value<0.01), and an increase in TNF- level. Simultaneous treatment with combined supplementation of vitamins E and D effectively stopped the decrease of TAC and the increase of TOS, OSI, and MDA. Although treatment with tamoxifen led to a decrease SOD, CAT, and GPX compared with group C, the difference wasn’t significant. Treatment with vitamins considerably caused to increase SOD and CAT activity in comparison with groups C and T. The current study’s findings demonstrated that the combined supplementation of vitamins E, and D effectively alleviated Tamoxifen-associated liver damage and oxidative stress.

The protective effects of vitamins E and D, stemming from their antioxidant and anti-inflammatory capabilities were investigated in the context of tamoxifen-induced liver toxicity. The study involved twenty-five female rats divided into five experimental groups: group C (olive oil: 500 L), group T (tamoxifen: 40 mg/kg), groups TE (tamoxifen: 40 mg/kg and vitamin E: 100 IU/kg), group TD (tamoxifen: 40 mg/kg and vitamin D: 500 IU/kg) and group TED (tamoxifen: 40 mg/kg, vitamin E: 100 IU/kg and vitamin D: 500 IU/kg). Calorimetric methods were used to measure biochemical variables, hepatic level of Total antioxidant capacity (TAC), Total oxidant status (TOS), Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx). Hepatic level of tumor necrosis factor- (TNF-) was assayed by ELISA.Hematoxylin-eosin staining method was also employed to assess Tamoxifen-induced liver lesions. Tamoxifen treatment resulted in a significant increase in ALP (p-value<0.01), TOS, and OSI (p-value<0.01), a marked decrease in TAC level (p-value<0.01), and an increase in TNF- level. Simultaneous treatment with combined supplementation of vitamins E and D effectively stopped the decrease of TAC and the increase of TOS, OSI, and MDA. Although treatment with tamoxifen led to a decrease SOD, CAT, and GPX compared with group C, the difference wasn’t significant. Treatment with vitamins considerably caused to increase SOD and CAT activity in comparison with groups C and T. The current study’s findings demonstrated that the combined supplementation of vitamins E, and D effectively alleviated Tamoxifen-associated liver damage and oxidative stress.

The protective effects of vitamins E and D, stemming from their antioxidant and anti-inflammatory capabilities were investigated in the context of tamoxifen-induced liver toxicity. The study involved twenty-five female rats divided into five experimental groups: group C (olive oil: 500 L), group T (tamoxifen: 40 mg/kg), groups TE (tamoxifen: 40 mg/kg and vitamin E: 100 IU/kg), group TD (tamoxifen: 40 mg/kg and vitamin D: 500 IU/kg) and group TED (tamoxifen: 40 mg/kg, vitamin E: 100 IU/kg and vitamin D: 500 IU/kg). Calorimetric methods were used to measure biochemical variables, hepatic level of Total antioxidant capacity (TAC), Total oxidant status (TOS), Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx). Hepatic level of tumor necrosis factor- (TNF-) was assayed by ELISA.Hematoxylin-eosin staining method was also employed to assess Tamoxifen-induced liver lesions. Tamoxifen treatment resulted in a significant increase in ALP (p-value<0.01), TOS, and OSI (p-value<0.01), a marked decrease in TAC level (p-value<0.01), and an increase in TNF- level. Simultaneous treatment with combined supplementation of vitamins E and D effectively stopped the decrease of TAC and the increase of TOS, OSI, and MDA. Although treatment with tamoxifen led to a decrease SOD, CAT, and GPX compared with group C, the difference wasn’t significant. Treatment with vitamins considerably caused to increase SOD and CAT activity in comparison with groups C and T. The current study’s findings demonstrated that the combined supplementation of vitamins E, and D effectively alleviated Tamoxifen-associated liver damage and oxidative stress.