Inhalation exposure to crude oil vapor induces behavioural deficits by increasing oxidative stress and histopathological changes in rat hippocampus: Quercetin therapeutic approach.

OBJECTIVE

Inhalation exposure to crude oil vapor (COV) and petroleum products is considered responsible for neurobehavioral toxicity in human and animal models. The antioxidant activity of quercetin (Que) and its derivatives are promising for protecting the hippocampus. This study aimed to evaluate the neuroprotective role of Que against COV-induced behavioral alterations and hippocampus damage.

METHODS

Eighteen adult male Wistar rats were randomly divided into the following three groups (n = 6): the control, the COV, and the COV + Que group. The inhalation method was used to expose the rats to crude oil vapors for 5 h daily, and Que (50 mg/kg) was administered orally. After 30 days of treatment, the spatial working memory and anxiety levels were evaluated using the cross-arm maze and elevated plus maze (EPM), respectively. TUNEL assay and hematoxylin-eosin (H&E) staining were used to identify the necrosis, normal and apoptotic cells in the hippocampus. Moreover, the levels of oxidative stress biomarkers including malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC) were investigated in the hippocampus tissue.

RESULTS

The results indicated that exposure to COV was associated with a significant decrease in spatial working memory and activity of CAT, TAC, SOD, and GPx enzymes compared to the control (P < 0.05). Moreover, COV significantly increased the level of anxiety, MDA, and hippocampal apoptosis (P < 0.05). The simultaneous administration of quercetin along with exposure to COV improved the behavioral alterations, activity of antioxidant enzymes, and hippocampal apoptosis.

CONCLUSIONS

These findings suggest that quercetin prevents COV-induced hippocampal damage by enhancing the antioxidant system and preventing cell apoptosis.