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hepatoprotective effect against dimethyl nitrosamine in metabolism. Se administration increases the antioxidant
[58]
intoxicated rats. Moreover, vitamin B suppresses genetic capacity of several intracellular systems. In addition, Se
12
expression of α-smooth muscle actin and heat-shock protein showed hepatoprotective effect against malathion-induced
47, which are markers of liver fibrosis. [44] liver injury and diabetic rats. [59,60] Table 2 demonstrated the
effect of micronutrients on hepatic lesions.
Vitamin C (ascorbic acid) is one of the most required nutrients
for a variety of biological functions. The health-promoting DIETARY SUPPLEMENTS
effects of vitamin C can be attributed to its biological
functions as a cofactor for a number of enzymes, most N-acetyl cysteine (NAC) is a derivative of the sulfur-containing
notably hydroxylases involved in collagen synthesis and amino acid cysteine and an intermediary (along with glutamic
as a water-soluble antioxidant. However, it can exert its acid and glycine) in the conversion of cysteine to GSH. Oral
[45]
antioxidant properties in both aqueous and non-aqueous NAC administration leads to an increase in intracellular
environments. Vitamin C is able to decrease hepatic cysteine and GSH levels. NAC is the primary antidote for
[61]
[46]
[62]
apoptosis and necrosis against cholestatic liver injury in acetaminophen-induced hepatotoxicity. NAC is able to
experimental animals. [47] inhibit genotoxicity due to reactive oxygen species (ROS),
protect DNA and nuclear enzymes, and prevent the
[63]
Vitamin E (α-tocopherol) is a potent lipid-soluble and formation of carcinogen-DNA adducts. NAC succeeded in
chain-breaking antioxidant required nutrient for humans the treatment of severe hepatic injury induced by a dietary
because it is necessary for the prevention of several fitness supplement. [64]
symptoms, including peripheral neuropathy and hemolytic
anemia. [48] It plays a significant role in preventing or Alpha lipoic acid (ALA) influences oxidative status by
minimizing peroxidation damage in biological systems. scavenging ROS, regenerating endogenous antioxidants,
[49]
[65]
Supplementation with vitamin E inhibits DNA damage due to repairing oxidative damage, and chelating metal ions.
free radical scavenging activity and its exerting anti-cytotoxicity ALA has been proven to be a natural, yet very powerful free
and anti-genotoxicity. [50,51] Moreover, α-tocopherol showed radical scavenger and antioxidant. ALA has a protective effect
hepatoprotective activity against cisplatin-induced oxidative against CCl -induced hepatotoxicity and prevents against liver
4
stress, which may be attributed to down-regulations of fibrosis due to inhibition of transforming growth factor (TGF)/
NADPH oxidase gene expression. [52] platelet-derived growth factor-stimulated HSCs activation
and ROS generation. [66-68]
Zinc (Zn) is an essential trace element with various biological
effects, depending on its catalytic and structural role in an L-carnitine (CAR) is a conditionally essential nutrient,
enormous number of enzymes and “Zn-finger” proteins. synthesized endogenously from lysine and methionine
[53]
Zn ions (Zn ) control cell proliferation, differentiation, and in the liver, kidney, and brain and it induces its effects
2+
have a role in both apoptotic and necrotic cell death. Zn on both fat and glucose metabolism. [69] CAR binds to
[54]
also has anti-oxidative and anti-inflammatory properties fatty acyl-coenzyme A and regulates their transport into
and it postulates hepatonephroprotective effect due to its mitochondrial matrix for β-oxidation. L-CAR is a superoxide
[70]
antioxidant, anti-apoptotic, and anti-inflammatory properties scavenger, antioxidant, and DNA cleavage protector. L-CAR
against cadmium-induced hepatotoxicity and reduction of has shown a protective effect against radiation-induced
metal accumulation in the organism, which may lead to
nephrotoxicity. [55,56] Table 2: Effect of micronutrients against hepatic injury
Name Mechanism of action Major effect
The naturally occurring element selenium (Se) plays a major Vitamin B 12 Suppresses genetic expression Hepatoprotective
role in a wide variety of biological processes in mammals. Se of α-smooth muscle actin and effect
heat-shock protein 47
acts as one of the major components due to its low molecular Inhibit hepatic fi brosis
weight as well as its presence within at least 25 proteins, Vitamin C Free radical scavenger Antioxidant,
named selenoproteins, in the form of the amino acid Vitamin E Prevention of tumor initiation anti-apoptosis
↓Genetic expression NADPH,
Anti-cytotoxicity and
selenocysteine, which is incorporated during translation and is DNA damage anti-genotoxicity
directly involved in redox catalysis. Although the function of Prevention of tumor initiation
[57]
most selenoproteins is still unknown, thioredoxin reductase, Zinc Free radical scavenger, control Anti-infl ammatory,
cell proliferation anti-apoptosis
GSH peroxidases, and thyroid hormone deiodinases are well Prevention of tumor initiation
described as selenoproteins, which is involved in maintaining Selenium Catalysis of redox reaction Antioxidant
the cell reduction-oxidation balance and thyroid hormone Prevention of tumor initiation

114 Hepatoma Research | Volume 1 | Issue 3 | October 15, 2015