article · Journal of Innovations in Medical Research
Acetaminophen overdose is a known cause of liver damage, driving the search for safer alternatives to synthetic protective treatments. An investigation evaluated the protective and curative potential of virgin coconut oil against acetaminophen-induced liver toxicity in thirty-six adult Wistar rats divided into twelve groups. Acetaminophen administration led to reduced body weight, enlarged liver weight, elevated liver enzymes such as alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase, as well as depleted antioxidant markers including glutathione peroxidase, superoxide dismutase, and catalase. Administering virgin coconut oil before or after acetaminophen exposure maintained liver enzymes within normal reference ranges and sustained normal antioxidant activity. It also supported healthy body weight and normal liver weight. These results indicate that virgin coconut oil counteracts acetaminophen-induced liver toxicity, providing both protective and curative actions in an animal model.
Acetaminophen is among the most widely used pain relievers globally, but high doses can cause severe liver injury. Identifying natural, accessible substances that can prevent or repair liver damage offers a pathway towards safer complementary therapies. This research indicates that virgin coconut oil can help mitigate the toxic effects of painkiller overdose on liver tissue and antioxidant defences.
The findings point towards the potential development of virgin coconut oil as a nutraceutical or therapeutic supplement to protect liver function during high-dose painkiller therapy. Pharmaceutical and nutritional supplement developers are the primary prospective users. However, this work represents early-stage animal research, meaning clinical trials in humans would be necessary before any commercial therapeutic formulation or dietary protocol could be established.
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Acetaminophen-induced hepatotoxicity is a well-documented consequence of acetaminophen overdose, necessitating the exploration of therapeutic interventions to develop safer alternatives to synthetic drugs. In this study, we investigated the potential effects of Virgin Coconut Oil (VCO) on acetaminophen (PCM)-induced hepatotoxicity. Thirty-six Wistar rats were divided into twelve groups as follows: Groups 1 and 2 received Normal Saline for 20 and 40 days, respectively; Groups 3 and 4 were administered 750mg/kg of PCM for 20 and 40 days, respectively. Group 5 received 2.5ml/kg of VCO for the initial 10 days followed by 750mg/kg of PCM for the subsequent 10 days. Group 6 received VCO at 2.5ml/kg for the first 20 days followed by 750mg/kg of PCM for the remaining 20 days. Groups 7 and 8 received VCO at 5ml/kg for the initial 10 and 20 days, respectively, followed by PCM administration for the subsequent 10 and 20 days. Groups 9 and 10 were administered 750mg/kg of PCM for the initial 10 and 20 days, respectively, followed by VCO at 2.5ml/kg for the remaining 10 and 20 days. Lastly, Groups 11 and 12 received 750mg/kg of PCM for the initial 10 and 20 days, respectively, followed by VCO at 5ml/kg for the remaining 10 and 20 days. Acetaminophen administration resulted in a significant (p≤0.05) decrease in the final body weight of PCM-treated groups, while a significant (p≤0.05) increase in body weight was observed in the negative control, pre-treated, and post-treated groups with VCO. Notably, PCM-treated groups exhibited a significant (p≤0.05) increase in liver weight compared to negative control and VCO-treated groups. Liver enzyme levels including ALP, ALT, AST, and GGT remained within normal reference ranges in negative control and VCO-treated groups, whereas a significant (p≤0.05) increase was observed in the positive control groups. Additionally, levels of GPx, SOD, and CAT were significantly (p≤0.05) decreased in the positive control group compared to the negative control and VCO-treated groups. Overall, the findings of this study demonstrate the potential ameliorating effect of VCO against PCM-induced liver toxicity, highlighting its potential therapeutic utility in mitigating hepatotoxicity.
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DOI: 10.63593/jimr.2788-7022.2025.08.004
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