Protection by turmeric and myrrh against liver oxidative damage and genotoxicity induced by lead acetate in mice.
The effects of lead acetate in the diet (0.5% w/w) on reduced GSH, activity of phase II metabolizing enzyme glutathione S-transferase (GST), lipid peroxidation in liver homogenate and bone marrow chromosomes of mice simultaneously supplemented with powdered turmeric and myrrh for 8 weeks were investigated. Five groups of Swiss male albino mice, each of 30 mice, the first group received a basal diet and served as negative control, the second group received basal diet supplemented with lead acetate only and served as positive control. The other three groups received basal diet supplemented with lead acetate and 1% or 5% turmeric powder and 1% myrrh powder, respectively. Results revealed a significant decrease in the amount of GSH in all treated groups compared with negative control. Also, the activity of GSH S-transferase was significantly decreased in positive control compared with other groups. However, co-administration of the protective plants resulted in a significant increase in the activity of GST compared with both positive and negative control groups. Furthermore, lipid peroxidation was significantly increased in positive control alone, while co-treatment with the protective plants resulted in reduction in the level of lipid peroxidation by 31% and 49% in mice receiving 1% and 5% turmeric powder respectively and 45% in 1% myrrh treated when compared with their respective positive control group. Lead genotoxicity was confirmed through significant reduction in the number of dividing cells, increased total number of aberrant cells and increased frequency of chromosomal aberrations. Simultaneous treatment with these plants significantly reduced the genotoxicity induced by lead administration and the powerful protection was observed with 5% powdered turmeric. It may be concluded that turmeric and myrrh are useful herbal remedies, especially for controlling oxidative damages and genotoxicity induced by lead acetate intoxication.
El-Ashmawy
Ibrahim M
IM
Department of Pharmacology, Faculty of Veterinary Medicine, Alexandria Univerity Research Development, Alexandria, Egypt.
Ashry
Khalid M
KM
El-Nahas
Abeer F
AF
Salama
Osama M
OM
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001854:Bone Marrow Cells / Q000187:drug effects* / Q000473:pathology; D049109:Cell Proliferation; D002869:Chromosome Aberrations; D029744:Commiphora; D030024:Curcuma; D019587:Dietary Supplements; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007855:Lead Poisoning / Q000503:physiopathology*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D009153:Mutagens / Q000633:toxicity; D009942:Organometallic Compounds / Q000633:toxicity; D018384:Oxidative Stress; D028321:Plant Preparations / Q000494:pharmacology*; D012116:Resins, Plant; D027343:Rhizome
D000975:Antioxidants; D009153:Mutagens; D009942:Organometallic Compounds; D028321:Plant Preparations; D012116:Resins, Plant; D005982:Glutathione Transferase; D005978:Glutathione; C008261:lead acetate