RESUMEN
BACKGROUND: An alarming number of zinc oxide nanoparticles (ZnO-NPs) have leaked into the environment, endangering the tissues of many living creatures, due to the recent surge in their use in several items. Through intra-peritoneal injection, this research intends to examine the impact of ZnO-NPs on the hepatic and gastrointestinal structures of male albino mice. METHOD: For seven and 14 days, animals were given 0.1 ml of 100 and 200 mg kg-1 of 50 nm-size ZnO-NPs, respectively. In contrast, those in the control group were given only water and food. RESULT: The results demonstrated that the treated mice's livers underwent functional changes and histological damage. After seven and 14 days, there was a notable rise in the average levels of the glutamate-oxaloacetate transaminase and glutamate-pyruvate transaminase enzymes in comparison to the control group (p≤0.05). Concentration time determines the magnitude of this impact. When enzyme levels vary, it means the liver isn't working properly. Histological changes in the liver, such as necrosis, destruction of hepatocyte membranes, widening of sinusoidal spaces and vacuolation of their cytoplasm, vascular congestion, and an increased number of Kupffer cells, were induced in mice treated with ZnO-NPs at two studied concentrations (100 and 200 mg/kg) for seven and 14 days, respectively. These effects were time-dose-dependent, according to the results of hematoxylin-eosin staining of liver tissue images.
RESUMEN
In fish, a complex set of mechanisms deal with environmental stresses including hypoxia. In order to probe the hypothesis that hypoxia-induced stress could be manifested in varieties of pathways, a model species, mirror carp (Cyprinus carpio), were chronically exposed to hypoxic condition (dissolved oxygen level: 1.80 ± 0.6 mg/l) for 21 days and subsequently allowed to recover under normoxic condition (dissolved oxygen level: 8.2 ± 0.5 mg/l) for 7 days. At the end of these exposure periods, an integrated approach was applied to evaluate several endpoints at different levels of biological organisation. These included determination of (i) oxidative damage to DNA in erythrocytes (using modified comet assay), (ii) lipid peroxidation in liver samples by measuring the malondialdehyde production using the 2-thiobarbituric acid [i.e. thiobarbituric acid reactive substances (TBARS) assay] and (iii) histopathological changes in gills. In addition, transcriptional expression of hypoxia-inducible factor 1 α (HIF-1α) and genes involved in the repair of oxidative damage to DNA (i.e. ogg1) and base excision repair (i.e. xrcc1) using reverse transcription polymerase chain reaction in liver samples were also determined. The results suggested significantly enhanced expression of these genes in response to hypoxia compared to concurrent normoxic controls. While the expression of HIF-1α reverted to control values within 7 days exposure to normoxic condition (P < 0.05), the transcriptional expression of the two genes involved in DNA repair process remained significantly high under the recovery period, which complemented the induction of oxidative damage to DNA. Hypoxic groups showed significantly increased values for TBARS level (~2-fold) and histopathological changes in gill tissues compared to both normoxic and recovery groups. Overall, oxidative damage to DNA determined by modified comet assay reflected the observed biological responses in other tissues of the fish. Along with other parameters, this integrated experimental design further strengthens the applications of the comet assay as an important technique to assess stress-induced DNA damage in ecotoxicological studies.
