Pomegranate juice treatment reverses carbon tetrachloride (CCl4)-induced increased acetylcholinesterase activity and cell death via suppression of oxidative stress in rats.

Background: Environmental pollution, including exposure to carbon tetrachloride (CCl4), poses serious health risks, particularly through oxidative stress, which may lead to neurodegenerative damage. Antioxidants, especially those found in natural products, show potential in mitigating these toxic effects. Pomegranate juice (PJ), rich in bioactive phytochemicals, has demonstrated antioxidant, anti-inflammatory, and neuroprotective properties.

Objective: This study aimed to investigate the protective effects of PJ on neurotoxicity induced by CCl4 in rats, assessing specific markers of oxidative stress, enzymatic activity, and apoptotic cell death.

Material and methods: Twenty-eight male Wistar rats were divided into four groups: Control, CCl4, PJ, and CCl4+PJ. The CCl4 group received intraperitoneal injections of CCl4 (0.2 ml/100 g) twice weekly for six weeks, while the PJ group received PJ orally (4 ml/kg) daily for 30 days. The CCl4+PJ group received both treatments in sequence. Brain tissues were analysed for malondialdehyde (MDA), reduced glutathione (GSH), acetylcholinesterase (AChE), glutathione S-transferase (GST), glutathione reductase (GR), and carboxylesterase (CaE) activity. Apoptotic cell death was assessed using TUNEL staining.

Results: CCl4 exposure resulted in a marked increase in MDA levels and AChE activity in brain tissue (p<0.05), alongside a significant decrease in reduced GSH levels and GST activity (p<0.05). Treatment with PJ significantly lowered MDA levels and AChE activity in the CCl4+PJ group compared to the CCl4 group (p<0.05). However, GSH levels and GST activity showed no significant changes in the CCl4+PJ group. TUNEL staining indicated a reduction in apoptotic cells in the CCl4+PJ group versus the CCl4 group, suggesting reduced cellular damage with PJ treatment (p<0.05).

Conclusions: PJ demonstrates neuroprotective potential against CCl4-induced oxidative stress and neurotoxicity in rats by reducing oxidative markers and apoptosis. These findings suggest that PJ could serve as a natural protective agent against neurodegenerative risks associated with environmental pollutants like CCl4.