article · International Journal of Human Anatomy
Ingesting zinc oxide nanoparticles can cause substantial toxic injury to the liver. An animal study using adult male albino rats investigated these damaging effects and assessed the protective capacity of vitamin E. Rats exposed solely to zinc oxide nanoparticles experienced highly significant reductions in body and liver weights. Microscopic and biochemical examinations showed congested blood vessels, disrupted liver cell architecture, bile duct hyperplasia, heightened collagen deposition around central veins, and increased levels of Caspase 3 alongside elevated liver enzymes, aspartate aminotransferase and alanine aminotransferase. In contrast, pre-treating animals with daily doses of vitamin E prior to nanoparticle exposure improved structural tissue organisation and restored biochemical parameters towards normal. The findings demonstrate that zinc oxide nanoparticles induce serious liver toxicity and that vitamin E pretreatment partially counters these adverse structural and biochemical changes.
Zinc oxide nanoparticles are widely utilised, yet their potential toxic effects upon ingestion raise serious health concerns. Demonstrating that an accessible antioxidant such as vitamin E can alleviate liver injury offers valuable insight into protective interventions for individuals at risk of accidental, environmental, or occupational nanoparticle toxicity.
This work represents early-stage animal research that could inform future protective supplements or clinical treatments for individuals exposed to nanomaterials. Potential users include occupational health providers and nutraceutical researchers. Because the findings are restricted to laboratory rodents, any practical therapeutic application or commercial protective formulation remains at a very early stage of investigation.
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Background: Oral ingestion of zinc oxide nanoparticles (ZnONPs) may lead to serious liver injury. Vitamin E (VE) is an important antioxidant factor that can reduce such damage. Aim: This study aimed to evaluate the possible changes that could take place in the liver of adult male albino rats after oral ingestion of ZnONPs and elucidate the potential protective role of VE against such damage. Material and Methods: Forty eight male albino rats were divided into four groups of 12 animals each. Group (1) served as control group and received normal saline. Group (2) “VE-treated” received 100 mg/kg/day of VE dissolved in normal saline by oral gavage for 21 days. Group (3) “ZnONPs-treated” received a daily dose of ZnONPs dispersed in the fresh sterilized physiological saline solution 1mg/kg for 5 constitutive days. Group (4) “concomitant ZnONPs and VE-treated” was pretreated with VE 100 mg/kg/day for 14 days followed by the same dose of ZnONPs as in group (3) for 5 days. The extent of hepatic damage was evaluated by histological and immunohistochemical examination of liver samples and serological analysis of liver enzymes. Results: Body weights and liver weights showed very highly significant decrease (P <0.001) in the ZnONPs-treated group. The histological results in ZnONPs-treated group revealed congested dilated central veins and blood sinusoids, loss of normal arrangement of hepatocytes and most of hepatocytes showed marked vacuolated cytoplasm with darkly stained nuclei. Portal area affection was in the form of congested dilated portal veins with bile duct hyperplasia and cellular infiltration. There was an increase in the mount of blue stained collagen fibers around central veins together with strong positive reaction for Caspase 3 in ZnONPs-treated group. Similarly biochemical analysis indicated that the levels of serum aminotransferase (AST &ALT) significantly increased in ZnONPs-treated group when compared with other groups. Rats pretreated with VE showed improvement of the histological findings and biochemical parameters. Conclusion: Ingestion of ZnONPs could be associated with serious liver affection and pretreatment with VE is suggested to induce some improvement of such deleterious changes.
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DOI: 10.14302/issn.2577-2279.ijha-18-2384
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