Protective Effect of Phyllanthus fraternus against Thioacetamide-Induced Mitochondrial Dysfunction.

Abstract

SummaryThe effect of administration of thioacetamide on rat liver mitochondrial functions and the protective effect of an aqueous extract of Phyllanthus fraternus against thioacetamide-induced damage were studied. When rats were treated with thioacetamide, the rate of mitochondrial respiration was decreased significantly with both NAD+ linked and FAD linked substrates, and the respiratory control ratio, an index of membrane integrity and the P/O ratio, a measure of phosphorylation efficiency, decreased significantly. Also, there was a significant decrease in the activities of NADH dehydrogenase, succinate cytochrome c reductase, and cytochrome oxidase; whereas succinate dehydrogenase was not affected. A significant decrease was seen in membrane potential and in the level of mitochondrial ATP. There was a significant decrease in the levels of phosphatidylcholine, phosphatidylethanolamine, and cardiolipin by thioacetamide treatment. The lipid peroxide level increased significantly in thioacetamide-treated rats. Administration of P. fraternus prior to thioacetamide treatment relieved the inhibition of all the parameters studied, and brought down the lipid peroxide levels significantly in liver homogenates and mitochondria. This study shows that P, fraternus protects against thioacetamide-induced toxicity by its ability to suppress the elevated lipid peroxide levels in the mitochondrial membrane.

The protein fraction of Phyllanthus niruri plays a protective role against acetaminophen induced hepatic disorder via its antioxidant properties

“…Venkateswaran et al (1987) reported that P. niruri inhibited the replication of woodchuck hepatitis virus in vivo and decreased its pathological effect on woodchuck liver. Human clinical studies have been carried out with P. niruri (Thyagarajan et al, 1988) and it has been shown that it has potent activity against various hepatic disorders such as viral hepatitis and toxicity caused by different drugs and environmental toxicants (Unander et al, 1995;Padma and Setty, 1999). However, the mechanisms responsible for this hepatoprotective action of P. niruri are not yet well defined.…”

Protective effect of Phyllanthus fraternus against allyl alcohol-induced oxidative stress in liver mitochondria

“…Administration of the aqueous extract of the Phyllanthus fraternus significantly decreased the thioacetamide (Padma and Setty, 1997) or carbon tetrachloride (Padma and Setty, 1999) induced lipid peroxidation in vivo and protected the liver from the hepatotoxin-induced toxicity. Co-administration of amla (Emblica officinalis) with dimethyl hydrazine significantly reduced the cytotoxic products such as MDA and conjugated dienes (Anila kumar et al, 2004).…”

“…It was reported earlier from our laboratory that mitochondrial dysfunction caused by the administration of an alcohol (Sebastian and Setty, 1999) or thioacetamide (Padma and Setty, 1997) or carbon tetrachloride (Padma and Setty, 1999) could be prevented by prior administration of aqueous extract of Phyllanthus fraternus. This study mainly involved on mitochondrial function and lipid peroxidation.…”

“…It was reported earlier from our laboratory that mitochondrial dysfunction caused by the administration of alcohol (Sebastian and Setty, 1999) or thioacetamide (Padma and Setty, 1997) or carbon tetrachloride (Padma and Setty, 1999) could be prevented by prior administration of an aqueous extract of Phyllanthus fraternus and the protective effect was attributed mainly to the antioxidant property of the extract. The main objective of the present study is to show the protective effect of the prior administration of Phyllanthus fraternus on the oxidative stress that is induced by the administration of allyl alcohol, which is known to deplete GSH.…”

Protective role ofPhyllanthus niruri against nimesulide induced hepatic damage

“…Although a number of reports described the usefulness of this herb against the adverse effects of various drug and toxicants (18)(19)(20)(21), no studies have been published to date, describing its beneficiary role against nimesulide-induced hepatotoxicity. The anti-inflammatory drug, nimesulide is a selective cyclooxygenase-2 (COX-2) inhibitor, with only residual activity against cyclooxygenase-1 (COX-1) (22,23).…”