Shaalan, S., Radwan, O., Saleh, H. (2017). ROLE OF WHEAT GERM OIL AGAINST CARBON TETRACHLORIDE-INDUCED NEUROTOXICITY IN BRAIN TISSUES OF ADULT MALE MICE. Egyptian Journal of Zoology, 67(67), 1-18. doi: 10.12816/0037791
Shebl Shaalan; Omyma K. Radwan; Hanan Saleh. "ROLE OF WHEAT GERM OIL AGAINST CARBON TETRACHLORIDE-INDUCED NEUROTOXICITY IN BRAIN TISSUES OF ADULT MALE MICE". Egyptian Journal of Zoology, 67, 67, 2017, 1-18. doi: 10.12816/0037791
Shaalan, S., Radwan, O., Saleh, H. (2017). 'ROLE OF WHEAT GERM OIL AGAINST CARBON TETRACHLORIDE-INDUCED NEUROTOXICITY IN BRAIN TISSUES OF ADULT MALE MICE', Egyptian Journal of Zoology, 67(67), pp. 1-18. doi: 10.12816/0037791
Shaalan, S., Radwan, O., Saleh, H. ROLE OF WHEAT GERM OIL AGAINST CARBON TETRACHLORIDE-INDUCED NEUROTOXICITY IN BRAIN TISSUES OF ADULT MALE MICE. Egyptian Journal of Zoology, 2017; 67(67): 1-18. doi: 10.12816/0037791
ROLE OF WHEAT GERM OIL AGAINST CARBON TETRACHLORIDE-INDUCED NEUROTOXICITY IN BRAIN TISSUES OF ADULT MALE MICE
1Zoology Department, Faculty of Science, Cairo University, Giza, Egypt
2Physiology Department, National Organization for Drug Control and Research, Giza, Egypt
Abstract
The present study aimed to evaluate the possible curative effect of wheat germ oil (WGO) against carbon tetrachloride (CCl4)-induced neurotoxicity accompanied to the oxidative stress in brain tissue of adult male mice. A total of 24 mice were divided into 4 groups, 6 animals for each group. Control group: received oral corn oil for 10 days (0.5 mL/kg body weight). Wheat germ oil (WGO) group: received corn oil (0.5 mL/kg body weight) orally for 2 days then WGO (1400 mg/kg body weight) for 8 days. Carbon tetrachloride (CCl4) group: received CCl4 in corn oil orally (0.5 mL/kg body weight) for 2 days then received corn oil (0.5 mL/kg body weight) for 8 days. WGO+ CCl4 group: received CCl4 in corn oil (0.5 mL/kg body weight) orally for 2 days then WGO (1400 mg/kg body weight) for 8 days. Administration of CCl4 induced increment in malondialdehyde (MDA), nitric oxide (NO), oxidized glutathione (GSSG), 8-hydroxy-2-deoxyguanosine (8-OHdG), adenosine di- and mono-phosphates (ADP & AMP), while caused drop in reduced glutathione (GSH), adenosine triphosphate (ATP) and monoamines in brain tissues. Administration of WGO could reduce neurotoxicity and mitochondrial dysfunction caused by CCl4. WGO exhibited curative effect in restoring energy production, improving oxidative status, reducing DNA degradation and modulating neurotransmitters levels. In conclusion, CCl4-induced neurotoxicity aggravated the oxidative stress in brain tissues, causing DNA fragmentation, inhibited energy production and suppressed monoamines release. One the other hand, administration of WGO attained improvement in the aforementioned negative changes.
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