Saturday, 21 August 2021

Tomato (Lycopersicon esculentum) Extracts Elicit Anti-Hepatotoxic Effects on Acetaminophen-Induced Liver Injury in Albino Wistar Rat | Chapter 4 | Technological Innovation in Pharmaceutical Research Vol. 10

 Introduction: Drug overdose is the largest cause of liver injury in the world today, according to numerous reports. Natural antioxidant-rich diets have been shown to provide significant relief from drug-induced organ damage.

The goal of this investigation was to see if tomato extract could protect rats from acetaminophen-induced acute hepatotoxicity.

Methods: Phytochemical tests were carried out. A total of 24 albino rats weighing 11010 g were divided into four groups (A-D), each with six rats. The usual control group, Group A, received no treatment. The negative control group got only a single dose of acetaminophen (750 mg/kg, i.p) as a single dose. The test group got a single dose of acetaminophen (750 mg/kg, i.p.) before receiving 14 days of therapy with tomato extract (30 mg/kg, oral). For 14 days, Group D was given tomato extract (30 mg/kg, oral) and acetaminophen (750 mg/kg, i.p) at the same time.

When compared to normal (p0.05 or p0.01), a single dosage of Acetaminophen induced liver cell damage and a significant increase in the levels of the liver enzymes: AST (67.6711.41U/L); ALT (46.3310.59U/L); and ALP (223.7023.31U/L) in rats in negative control. On the liver enzyme marker levels, daily injection of tomato extract was able to reduce the acetaminophen-induced hepatotoxicity: AST (23.00 3.61U/L, P0.01), ALT (17.67 3.48U/L, P0.05), and ALP (121.308.11U/L, P0.01) were all higher in Group C. When compared to the negative control group, AST (26.672.91U/L, P0.01), ALT (18.671.76 U/L, P0.05), and ALP (124.729.33U/L, P0.01) were significantly higher in Group D. In comparison to the normal control group, histological data demonstrated no substantial liver injury in the tomato extract groups.

Tomato extract has hepatoprotective properties against acetaminophen-induced liver damage.

Author (S) Details

I. K. Uchendu
Department of Medical Laboratory Science, Division of Clinical Chemistry, University of Nigeria, Enugu Campus, Enugu State, Nigeria.

C. E. Agu
Department of Medical Laboratory Science, Division of Clinical Chemistry, University of Calabar, Nigeria.

O. C. Orji
Department of Medical Laboratory Science, Division of Clinical Chemistry, University of Nigeria, Enugu Campus, Enugu State, Nigeria.

E. B. Nnedu
Department of Medical Laboratory Science, Division of Immunology, University of Nigeria, Enugu Campus, Nigeria.

C. Arinze
Department of Medical Laboratory Science, Division of Clinical Chemistry, University of Nigeria, Enugu Campus, Enugu State, Nigeria.

A. C. Uchenna
Department of Medical Laboratory Science, Division of Medical Microbiology, University of Nigeria, Enugu Campus, Enugu State, Nigeria.

U. C. Okongwu
Department of Medical Laboratory Science, Division of Medical Microbiology, University of Nigeria, Enugu Campus, Enugu State, Nigeria.

View Book :- https://stm.bookpi.org/TIPR-V10/article/view/2841

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