Ameliorative role of ethanolic extract of Moringa oleifera leaf on aflatoxin B1-induced genotoxicity and biochemical alterations in rats
Journal of the Arab Society for Medical Research. 2018; 13 (1): 60-70
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Background/aim: the present study was conducted to assess the ameliorative role of Moringa oleifera leaf extract [MOLE] on genotoxicity and biochemical alteration of aflatoxin B1 [AFB1] in rats
Materials and methods: the rat groups involved negative control, control of DMSO, positive control that received AFB1 in DMSO [0.7 g/kg, body weight] four times weekly for 1 month, groups 4-6 that received the same dose of AFB1 in DMSO at the same period plus MOLE doses [3.3, 4.0 and 4.7 g/kg] daily for 1 month, and groups 7-9 that received MOLE alone at the same doses for 15 days after cessation of AFB1 treatment. Molecular genetic, cytogenetic, sperm, and biochemical studies were documented
Results: genetic and sperm results revealed that AFB1 treatment induced significant elevation of genetic alterations and sperm abnormalities as compared with normal control. Biochemical studies showed that the treatment with AFB1 disturbed the parameters of liver functions, where aspartate-transaminase, alanine-transaminase, and alkaline phosphatase were activated and bilirubin contents as well as the rate of malondialdehyde were increased significantly, but the endogenous antioxidative system [catalase, superoxide-dismutase activities and glutathione as well as total antioxidant capacity] and protein profile were reduced significantly. Moreover, kidney functions [urea, uric acid, and creatinine contents] were elevated under AFB1 administration. The treatment with MOLE significantly minimizes the genetic alterations, sperm abnormalities, and biochemical destruction. These ameliorations were increased by increasing the dose level. Better findings were seen by using MOLE as a therapeutic agent than its using as a protective agent
Conclusion: this study revealed that MOLE contains therapeutic factors used in curing of genotoxicity induced by AFB1 in rats, and treatment of animals that were exposed to AFB1 with MOLE significantly ameliorated the genetic, sperm, and biochemical parameters as compared with animals treated with AFB1 alone
Materials and methods: the rat groups involved negative control, control of DMSO, positive control that received AFB1 in DMSO [0.7 g/kg, body weight] four times weekly for 1 month, groups 4-6 that received the same dose of AFB1 in DMSO at the same period plus MOLE doses [3.3, 4.0 and 4.7 g/kg] daily for 1 month, and groups 7-9 that received MOLE alone at the same doses for 15 days after cessation of AFB1 treatment. Molecular genetic, cytogenetic, sperm, and biochemical studies were documented
Results: genetic and sperm results revealed that AFB1 treatment induced significant elevation of genetic alterations and sperm abnormalities as compared with normal control. Biochemical studies showed that the treatment with AFB1 disturbed the parameters of liver functions, where aspartate-transaminase, alanine-transaminase, and alkaline phosphatase were activated and bilirubin contents as well as the rate of malondialdehyde were increased significantly, but the endogenous antioxidative system [catalase, superoxide-dismutase activities and glutathione as well as total antioxidant capacity] and protein profile were reduced significantly. Moreover, kidney functions [urea, uric acid, and creatinine contents] were elevated under AFB1 administration. The treatment with MOLE significantly minimizes the genetic alterations, sperm abnormalities, and biochemical destruction. These ameliorations were increased by increasing the dose level. Better findings were seen by using MOLE as a therapeutic agent than its using as a protective agent
Conclusion: this study revealed that MOLE contains therapeutic factors used in curing of genotoxicity induced by AFB1 in rats, and treatment of animals that were exposed to AFB1 with MOLE significantly ameliorated the genetic, sperm, and biochemical parameters as compared with animals treated with AFB1 alone
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Índice:
IMEMR
Idioma:
En
Revista:
J. Arab Soc. Med. Res.
Ano de publicação:
2018