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

Ömer Faruk Kalkan, Ahmet Türk, Cihan Çitil, Miraç Uçkun, Ahmet Özkaya, Ertan Yoloğlu, Yusuf Özay, Şeyda Çağri Bülbül, Zafer Şahin, Akın Kirbaş
Author Information
  1. Ömer Faruk Kalkan: Department of Physiology, Karadeniz Technical University Faculty of Medicine, Trabzon, Turkey.
  2. Ahmet Türk: Department of Histology and Embryology, Faculty of Medicine, Adiyaman University, Turkey.
  3. Cihan Çitil: Department of Biology, Faculty of Science and Art, Çankırı Karatekin University, Turkey.
  4. Miraç Uçkun: Department of Food Engineering, Faculty of Engineering, Adiyaman University, Turkey.
  5. Ahmet Özkaya: Department of Chemistry and Chemical Processing Techniques, Vocational School of Technical Sciences, Adıyaman University, Turkey.
  6. Ertan Yoloğlu: Department of Science Education, Faculty of Education, Adiyaman University, Turkey.
  7. Yusuf Özay: Department of Medical Biology and Genetics, Faculty of Medicine, Adiyaman University, Turkey.
  8. Şeyda Çağri Bülbül: Department of Chemistry, Faculty of Science and Art, Adiyaman University, Turkey.
  9. Zafer Şahin: Department of Physiology, Karadeniz Technical University Faculty of Medicine, Trabzon, Turkey.
  10. Akın Kirbaş: Faculty of Veterinary Medicine, Veterinary Internal Diseases, Atatürk University, Turkey.

Abstract

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.

Keywords

MeSH Term

Animals
Oxidative Stress
Rats
Rats, Wistar
Pomegranate
Fruit and Vegetable Juices
Male
Carbon Tetrachloride
Acetylcholinesterase
Antioxidants
Apoptosis
Neuroprotective Agents
Cell Death

Chemicals

Carbon Tetrachloride
Acetylcholinesterase
Antioxidants
Neuroprotective Agents

Word Cloud

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