الفهرس 
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Abstract
Acute Liver Failure is progressive evolvement of ALI accompanied with significant disruption of liver synthetic and metabolic functions and sudden development of hepatocellular necrosis. Thereby, an acutely injured liver fails to perform such important physiological functions essential for human body with an ultimate result of hepatic failure and death. In the current study, the research protocol placed an emphasis on assessing the feasibility of prevention of ALI in susceptible individuals. The patterns of necrosis and phagocytosis process were used to evaluate the potential cytoprotective activity of the compounds under investigation. Methyl palmitate and tiron were administrated orally to follow the same clinical pattern in humans and once daily for 8 days prior to the induction of liver injury. Methyl palmitate may have manifested hepatoprotective potential by either directly inhibiting the function of kupffer cells or by downregulating the expression of inflammatory mediators such as IL-6. In addition, methyl palmitate had a prominent role in preventing the oxidative stress inflicted by the toxicant and enhancing host- antioxidant defense. Tiron’s ability to prevent ALI apparently originated from its anti-oxidant and immune-modulatory properties. It significantly increased the anti-oxidant markers and downregulated IL-6 expression with subsequent reduction in both inflammatory response and oxidative stress. We assume that the oil-solubility of methyl palmitate enabled it to target extracellular free radicals in membrane phospholipids, while the water- solubility of tiron allowed it to scavenge intracellular free radicals.