Abstract
The possible protective effects of an aqueous rooibos extract (Aspalathus linearis), red palm oil (RPO) (Elaeis guineensis), or their combination on tert-butyl-hydroperoxide-(t-BHP-)induced oxidative hepatotoxicity in Wistar rats were investigated. tert-butyl hydroperoxide caused a significant (P < 0.05) elevation in conjugated dienes (CD) and malondialdehyde (MDA) levels, significantly (P < 0.05) decreased reduced glutathione (GSH) and GSH : GSSG ratio, and induced varying changes in activities of catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase in the blood and liver. This apparent oxidative injury was associated with histopathological changes in liver architecture and elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). Supplementation with rooibos, RPO, or their combination significantly (P < 0.05) decreased CD and MDA levels in the liver and reduced serum level of ALT, AST, and LDH. Likewise, changes observed in the activities of antioxidant enzymes and impairment in redox status in the erythrocytes and liver were reversed. The observed protective effects when rooibos and RPO were supplemented concomitantly were neither additive nor synergistic. Our results suggested that rooibos and RPO, either supplemented alone or combined, are capable of alleviating t-BHP-induced oxidative hepatotoxicity, and the mechanism of this protection may involve inhibition of lipid peroxidation and modulation of antioxidants enzymes and glutathione status.
Highlights
The liver is a target organ for toxic substances because the hepatocytes that make up the majority of the liver structure are very active in the metabolism of xenobiotics
Overproduction of ROS arising from mitochondrial electron transport chain or excessive stimulation of nicotinamide adenine dinucleotide phosphate-reduced tetrasodium salt (NADPH) results in oxidative stress, a deleterious process that can lead to damage to important cell structures, including lipids and membranes, proteins, and DNA [1, 3]. tert-butyl hydroperoxide (t-BHP) is a wellknown oxidant that has been used as a model to investigate mechanisms of cellular damage caused by oxidative stress [4,5,6,7]
Our results indicated that co-supplementation of rooibos and red palm oil (RPO) protects against t-BHP-induced hepatotoxicity as demonstrated by reduction in level of liver function marker enzymes, inhibition of conjugated dienes (CD) and MDA formation, reversal of changes in antioxidant enzymes, and increase in intracellular GSH level and GSH : GSSG ratio in t-BHPtreated rats
Summary
The liver is a target organ for toxic substances because the hepatocytes that make up the majority of the liver structure are very active in the metabolism of xenobiotics. Reactive oxygen and nitrogen species (RONS) are generated which can result in oxidative or nitrosative stress. Both ROS and RNS are products of normal cellular metabolism and they may be deleterious or beneficial species. Overproduction of ROS arising from mitochondrial electron transport chain or excessive stimulation of NADPH results in oxidative stress, a deleterious process that can lead to damage to important cell structures, including lipids and membranes, proteins, and DNA [1, 3]. It can be metabolized to peroxyl and alkoxyl radicals by cytochrome P-450 in the hepatocytes, which in turn can initiate lipid peroxidation, producing loss of membrane fluidity, and mediating DNA damage [4, 8], which
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