Abstract

Human and animal studies have shown that some drugs and chemical agents have potential hepatotoxic effects. The hepatotoxic effect of drugs and some chemical agents is reported to be associated with the generation of reactive oxygen species (ROS). These ROS are reported to be associated with lipid peroxidation in the liver. This mechanism has led to continuous evaluation of the hepatoprotective effect of antioxidants in humans and animals. Among the antioxidants been evaluated is vitamin C which is a water soluble antioxidant. Reports have linked vitamin C with hepatoprotective property in animals and humans. It synergistic hepatoprotective effect with other antioxidants was also reported. Due to these reports a comprehensive literature review on the hepatoprotective property of vitamin C in humans and animals was performed. It was observed that vitamin C exhibited a reputable hepatoprotective effect in humans and animals. Research showed that vitamin C inhibited hepatotoxicity induced by drugs, heavy metals, organophosphate insecticides and some chemical agents. Vitamin C was reported to normalized levels of serum alanine aminotransferase, aspartate aminotransferase, gamma glutamine, alkaline phosphatase, lactate dehydrogenase and malondialdehyde and serum bilirubin in intoxicated animals. It potentiates the activities of free radical scavengers, superoxide dimutase, and catalase glutathione peroxidase thereby preventing microsomal lipid peroxidation, liver fibrosis, liver necrosis and hepatic inflammation. In humans vitamin C was reported to be beneficial in non alcoholic steatohepatitis and in patients with fatty liver disease. Hepatoprotective property of vitamin C is attributed to it antioxidant property. Vitamin C (ascorbic acid) which is a major water-soluble antioxidant is believed to decrease lipid peroxidation either directly or indirectly by regenerating vitamin E. Vitamin C is an important free radical scavenger in extracellular fluids, trapping radicals and protecting biomembranes from peroxide damage. Vitamin C effectively scavenges singlet oxygen, superoxide, hydroxyl, water soluble peroxyl radical and hypochlorous acid. It is also reported to be an excellent source of electrons and therefore can donate electrons to free radicals such as hydroxyl and super oxide radicals and quench their activity. Vitamin C is an essential co-factor involved in many biochemical functions and acts as an electron donor or reducing agent. In this review it is observe that vitamin C has hepatoprotective effect which increases when co administered with other agents precisely antioxidants.

Highlights

  • Vitamin C was discovered by Szent-Gyorgyi (1928) [1]

  • It was observed that vitamin C exhibited a reputable hepatoprotective effect in humans and animals

  • It potentiates the activities of free radical scavengers, superoxide dimutase, and catalase glutathione peroxidase thereby preventing microsomal lipid peroxidation, liver fibrosis, liver necrosis and hepatic inflammation

Read more

Summary

Introduction

Vitamin C was discovered by Szent-Gyorgyi (1928) [1]. It is a six-carbon compound structurally related to glucose, consisting of two inter-convertible compounds: Lascorbic acid, which is a strong reducing agent, and its oxidized derivative, L dehydroascorbic acid. Vitamin C was reported to attenuate hepatic damage induced by some chemical agents especially in animals. They reported that vitamin C normalized levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, blood hydroperoxide and malondialdehyde in liver of carbon tetrachloride intoxicated rats. The hepatoprotective effect of vitamin C against organophosphate induced liver damage can be further buttress by the findings of Mossa et al (2011) [21].

Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.