Abstract

This study investigates the comparative hepatoprotective activity of crude ethanol extracts of Cuscuta australis against acetaminophen (APAP) intoxication. Thirty-six rats were randomly divided into six groups of 6 replicates: Group 1 which served as control received water. Group 2 was orally administered 835 mg/kg body wt. of paracetamol on day 8. Groups 3 and 4 were orally administered ethanolic extracts of the seed of Cuscuta australis in doses of 125 mg/kg and 250 mg/kg, respectively, for 7 days and then intoxicated as in Group 2 on the 8th day. Groups 5 and 6 received similar oral doses of Cuscuta australis stem extracts for 7 days and then intoxicated as in Groups 3 and 4. Group 2 rats showed severe periportal hepatic necrosis, significantly elevated serum hepatic injury markers, markedly increased lipid peroxidation, and decreased hepatic antioxidant enzymes activities. Remarkably, Cuscuta australis (seed and stem) extract pretreatments in Groups 3, 4, 5, and 6, most especially, the stem extract pretreatment in Groups 5 and 6, improved better the hepatic histoarchitecture, the hepatocellular, and the oxidative stress injury markers in a dose-dependent manner. Conclusively, ethanol extractions of Cuscuta australis stem appear to protect the liver from acetaminophen intoxication better than the seed counterpart.

Highlights

  • Acetaminophen (APAP) is a commonly used antipyretic analgesic drug for curing fever, headache, and other pains and is readily available without prescription

  • Which covalently bind to cellular macro molecules to produce protein adduct that culminates in acute hepatic necrosis [4,5,6]

  • The profile of CAT, superoxide dismutase (SOD), and GSH-PX enzymes of C. australis stem extracts was similar to its seed counterpart but a significantly (P < 0.01) dose-dependent response was observed in the stem extract pairs

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Summary

Introduction

Acetaminophen (APAP) is a commonly used antipyretic analgesic drug for curing fever, headache, and other pains and is readily available without prescription. The liver plays significant role in the metabolism of toxic chemicals, certain drugs, and environmental pollutants by using cytochrome P450 pathway. The latter convert acetaminophen to a highly toxic metabolite, N-acetyl-p-benzoquinamine (NAPQI) which under normal conditions is readily detoxified by conjugation with glutathione (GSH) [2, 3]. Oxidative stress is usually occasioned by increased level of this highly reactive species, NAPQI, and may contribute to the APAP hepatotoxicity via lipid peroxidation, mitochondrial damage, and ATP depletion [7]. Striking balance between reactive species and antioxidant enzymes might be a critical mechanism for ameliorating damage by oxidative stress under APAP toxicity [8]. There is no scientific documentation on the ameliorative potential of C. australis on acetaminopheninduced hepatotoxicity; this study seeks to investigate the possibility

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