Liver Disease Case Studies

1. Introduction

Liver disease represents a considerable public health burden that involves several etiologies overlapping symptoms (El-Serag & Rudolph, 2007). Since the seventies, the experimental model of carbon tetrachloride (CCl4) hepatotoxicity have been closely studied using in vivo models of acute and chronic liver injury. This process has been used comprehensively to examine the pathogenesis of liver injury such as centrilobular steatosis, inflammation, apoptosis and necrosis. CCl4 deteriorates hepatocytes directly by altering the permeability of the plasma, lysosomal, and mitochondrial membranes through initiation of lipid peroxidation with trichloromethyl radical (CCl3•) or trichloroperoxyl radical (CCl3OO•) by the hepatic microsomal cytochrome P450 oxygenase system. Oxidative stress and membrane damage in hepatocytes are mainly caused

SOD activity was calculated in terms of units/mg protein.
Total protein thiols (TPT) - This assay is based on the principle of formation of relatively stable yellow color by sulphydryl groups with DTNB (Moron et al., 1979). Briefly, 0.2 ml of liver homogenate was mixed with phosphate buffer (pH 8.0), 40 µl of 10 mM DTNB and 3.16 ml of methanol. This mixture was incubated for 10 min and the absorbance was measured at 412 nm against appropriate blanks. The total thiol content was calculated by using ε=13.6x10 cm-1 M-1 Sedlak & Lindsy, 1978).

2.11. Statistical analysis
Data were analyzed using StatSoft STATISTICA version 12 software. Differences between the groups were assessed by a nonparametric Mann–Whitney and Kruskal–Wallis tests. Values in the text are means±standard deviation (SD). Differences with p0.05 were considered to be statistically