This study examines the antioxidant potentials and also the ability of the aqueous extract of Tithonia diversifolia (Hemsl.) A. Gray leaves to inhibit some pro-oxidants (Fe 2+ and sodium nitroprusside) induced lipid peroxidation in rat's brain homogenates in vitro . The ability of the extracts to inhibit 25 μM FeSO 4 and 7.0 μM sodium nitroprusside induced lipid peroxidation in isolated rat's brain determined. The antioxidative potentials of the extract as typified by the overall phenol content, reducing power, 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging ability and iron II chelating ability were cojointly determined. The results of the study discovered that each pro-oxidant (Fe 2+ and sodium nitroprusside) caused a considerably increase in (p < 0.05) malonaldehyde (MDA) content of the brain. Though, aqueous extracts of Tithonia diversifolia caused a substantial concentration-dependent decrease (p < 0.05) within the malonaldehyde (MDA) contents of the brain. Though, aqueous extracts from Tithonia diversifolia had an appreciably higher (p < 0.05) inhibitory impact on each Fe 2+ and sodium nitroprusside induced lipid peroxidation within the rat's brain homogenates. This higher inhibitory effect of Tithonia diversifolia may be attributed to its considerably higher (p < 0.05) total phenol content, iron (II) chelating ability, reducing power and free radical scavenging ability. Therefore, Fe 2+ and sodium nitroprusside induced oxidative stress within the brain may be probably managed by dietary intake of Tithonia diversifolia leaves. These antioxidant potentials of T. diversifolia extract could have contributed to the employment of the leaves in the management of disease.
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