Antioxidant and inhibitory effect of red ginger (Zingiber officinale var. Rubra) and white ginger (Zingiber officinale Roscoe) on Fe(2+) induced lipid peroxidation in rat brain in vitro.
Neurodegerative diseases have been linked to oxidative stress arising from peroxidation of membrane biomolecules and high levels of Fe have been reported to play an important role in neurodegenerative diseases and other brain disorder. Malondialdehyde (MDA) is the end-product of lipid peroxidation and the production of this aldehyde is used as a biomarker to measure the level of oxidative stress in an organism. The present study compares the protective properties of two varieties of ginger [red ginger (Zingiber officinale var. Rubra) and white ginger (Zingiber officinale Roscoe)] on Fe(2+) induced lipid peroxidation in rat brain in vitro. Incubation of the brain tissue homogenate in the presence of Fe caused a significant increase in the malondialdehyde (MDA) contents of the brain. However, the aqueous extract from both varieties of ginger caused a significant decrease in the MDA contents of the brain in a dose-dependent manner. However, the aqueous extract of red ginger had a significantly higher inhibitory effect on both Fe(2+)-induced lipid peroxidation in the rat brain homogenates than that of white ginger. This higher inhibitory effect of red ginger could be attributed to its significantly higher phytochemical content, Fe(2+) chelating ability, OH scavenging ability and reducing power. However, part of the mechanisms through which the extractable phytochemicals in ginger (red and white) protect the brain may be through their antioxidant activity, Fe(2+) chelating and OH scavenging ability. Therefore, oxidative stress in the brain could be potentially managed/prevented by dietary intake of ginger varieties (red ginger and white ginger rhizomes).
Oboh
Ganiyu
G
Department of Biochemistry, Federal University of Technology, Akure, Ondo-State, Nigeria. goboh2001@yahoo.com
Akinyemi
Ayodele J
AJ
Ademiluyi
Adedayo O
AO
D000818:Animals; D000975:Antioxidants / Q000302:isolation & purification / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000302:isolation & purification; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002712:Chlorides / Q000737:chemistry; D005290:Ferric Compounds / Q000737:chemistry; D005296:Ferrous Compounds / Q000737:chemistry / Q000633:toxicity; D005419:Flavonoids / Q000302:isolation & purification; D020939:Zingiber officinale / Q000737:chemistry*; D066298:In Vitro Techniques; D007502:Iron Chelating Agents / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D010084:Oxidation-Reduction; D019800:Phenol / Q000302:isolation & purification; D010936:Plant Extracts / Q000302:isolation & purification / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D027343:Rhizome / Q000737:chemistry
D000975:Antioxidants; D002712:Chlorides; D005290:Ferric Compounds; D005296:Ferrous Compounds; D005419:Flavonoids; D007502:Iron Chelating Agents; D010936:Plant Extracts; D019800:Phenol; C020748:ferrous sulfate; D001205:Ascorbic Acid; C024555:ferric chloride