The Alleviative Efficacy of Vitamins A, C, and E Against Zinc Oxide Nanoparticles-Induced Hepatic Damage by Reducing Apoptosis in Rats.

Nanoparticles are vastly exploited in today's technology. However, it is realized that exposure to high concentrations of nanoparticles (NPs) may have adverse effects on human health. According to previous reports, zinc oxide (ZnO) NPs cause toxic effects in tissues via inducing apoptosis. The current work was designed to evaluate possible protective activities of vitamins (Vits) A, C, and E against ZnO NPs-induced apoptosis in the liver of rats. To this aim, fifty-four adult male Wistar rats were randomly distributed into nine groups (n = 6 rats for each group), namely, Control1 (water), Control2 (olive oil), Vit A (1000 IU/kg), Vit C (200 mg/kg), Vit E (100 IU/kg), ZnO (200 mg/kg), ZnO + VitA, ZnO + VitC, and ZnO + VitE. To investigate apoptosis, the mRNA and protein expression of Bcl-2-associated X (Bax) and B-cell lymphoma protein 2 (Bcl-2) were examined by qRT-PCR and western blot techniques. The mRNA and protein expression of TNF-α as well as the activity of caspase 3,7 were also measured. The results revealed that ZnO NPs considerably enhance the ratio of Bax to Bcl-2 mRNA and protein expression as well as the activity of caspase 3,7 compared to the control group. Furthermore, the findings implied that the elevated level of TNF-α may link with ZnO NPs-mediated apoptosis in the liver of rats. More importantly, Vits A, C, and E exhibited ameliorative properties against apoptosis-inducing effects of ZnO NPs. Thus, administration of Vits A, C, and E may be effective in preventing liver damage and apoptosis caused by ZnO NPs.

Vitamins A, C, and E Exert Anti-apoptotic Function in the Testis of Rats After Exposure to Zinc Oxide Nanoparticles.

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.

Ameliorative Effects of Vitamins A, C, and E on Sperm Parameters, Testis Histopathology, and Oxidative Stress Status in Zinc Oxide Nanoparticle-Treated Rats.

One of the most often utilized nanoparticles (NPs) in several technologies is zinc oxide (ZnO) NPs. However, these NPs are said to have harmful effects on the reproductive system. Thus, we designed this study to specify the potential preventive activity of vitamins (Vits) A, C, and E, as antioxidants, against toxicity of ZnO NPs in the testes of rats. A total of 54 Wistar rats were arranged in 9 groups of 6 and then orally received water (control 1), olive oil (control 2), Vit A (1000 IU/kg), Vit C (200 mg/kg), Vit E (100 IU/kg), ZnO (200 mg/kg), ZnO+Vit A, ZnO+Vit C, and ZnO+Vit E. To determine the amount of testicular injury, sperm analysis and histological evaluation were performed. In addition, oxidative stress status was examined using colorimetric and qRT-PCR methods. Our findings suggest that ZnO NPs cause adverse effects on sperm parameters and testicular histology. Furthermore, oxidative biomarkers (malondialdehyde and total oxidant capacity) were enhanced in the ZnO group. By contrast, the gene expression and activities of antioxidant enzymes (SOD, GPx, and CAT) noted a remarkable decrease in the ZnO group regarding control (p < 0.05). However, oxidative markers were remarkably mitigated after combined treatment of ZnO NPs and Vits A, C, or E compared to the rats given ZnO NPs (p < 0.05). Additionally, compared to the ZnO NP group, the rats receiving Vits+ZnO NPs exhibit increased antioxidant enzyme activity and mRNA expression (p < 0.05). The findings demonstrate the abovementioned Vits' ameliorative effects on toxicity incurred by ZnO NPs.

The Restoring Effect of Human Umbilical Cord-Derived Mesenchymal Cell-Conditioned Medium (hMSC-CM) against Carbon Tetrachloride-Induced Pulmonary Fibrosis in Male Wistar Rats.

Objective: Pulmonary toxicity induced by CCl4, a model of idiopathic pulmonary fibrosis (IPF), leads to tissue remodeling and inflammation. Human umbilical cord mesenchymal cell-conditioned medium (hMSC-CM) is a potent anti-inflammatory, antioxidative, and antifibrotic agent. Methods: Forty male Wistar rats were assigned to the control (C), olive oil control (C.O) (hMSC-CM), control (C.Ms), fibrosis (fb), and fibrosis with hMSC-CM (f.Ms) treatment groups. The groups C, C.O, and C.Ms received PBS (200 µl), olive oil (1 ml/kg), and hMSC-CM (100 µg protein/kg), respectively. The fibrosis group was administered with only CCl4 (1 ml/kg). The last group, f.Ms was treated with CCl4 (1 ml/kg) and 100 µg protein/kg IV hMSC-CM. While the treatment with olive oil and CCl4 was performed for 2 days/week from the first week for 12 weeks, the treatment with PBS and hMSC-CM was carried out 2 days/week from week 4th to week 12th. The effect of the UC-MSC culture medium treatment on the lung was evaluated by assessing lysyl oxidase (LOX), tumor necrosis factor-alpha (TNF-α), and transforming growth factor-ß1 (TGF-ß1) genes, and proteins expression by real-time RCR and western blotting, respectively. Results: Lysyl oxidase (LOX), tumor necrosis factor-alpha (TNF-α), transforming growth factor-b1 (TGF-ß1), malondialdehyde (MDA), and oxidative stress levels were markedly higher in the fibrosis group than in the control groups (p ≤ 0.001). Additionally, glutathione (GSH) in the fibrosis group was markedly lower than those in the control groups (p ≤ 0.001). Fibrosis in the UC-MSC treatment group had milder histopathological injuries than in the fibrosis group. Conclusion: hMSC-MSC as a strong anti-inflammatory, antioxidative, and antifibrotic decreases the level of oxidative stress, proinflammatory cytokines, and MDA causing a restoring effect against CCl4-induced pulmonary fibrosis.