The Alleviative Efficacy of Vitamins A, C, and E Against Zinc Oxide Nanoparticles-Induced Hepatic Damage by Reducing Apoptosis in Rats.
Biol Trace Elem Res
; 201(3): 1252-1260, 2023 Mar.
Article
em En
| MEDLINE
| ID: mdl-35364806
ABSTRACT
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.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Óxido de Zinco
/
Nanopartículas
Limite:
Adult
/
Animals
/
Humans
/
Male
Idioma:
En
Revista:
Biol Trace Elem Res
Ano de publicação:
2023
Tipo de documento:
Article