Int. J. Environ. Res. Public Health 2010, 7 1878 while C5 was involved in inflammation and injury to hepatocytes [28]. Another study demonstrated that NK cells may also directly ameliorate hepatic fibrosis, first by releasing antifibrotic cytokines (interferon [IFN]α and IFNγ), and second by killing activated stellate cells. Ethanol impairs the ability of NK cells to kill activated HSC. As a result, it could remove this break in the development of fibrosis (Figure 2) [29]. Figure 2. NK Natural killer, TNF- Tumor Necrosis Factor alpha, LPS Lipopolysaccharide. Moreover, there are some underlying conditions in which ethanol can cause damage in a broader manner. Thereby, ethanol and chronic HCV infection synergistically accelerate liver injury. The process by which this occurs remains unclear, but it is believed that chronic liver inflammation is the keyhole to this pathogenesis. In these cases, there is a relationship between increased alcohol intake and decreased response to interferon (IFN) therapy for HCV [7]. Chronic consumption of alcohol elevates iron levels in the body, not only when consuming iron-rich beverages like wine, but also stimulating exogenous iron absorption from food. In general, cells have protective mechanisms to attenuate harm caused by ROS and the oxidative process. These mechanisms include enzymes like SOD (Superoxide Dismutase), catalase, glutathione peroxidase (which removes H2O2), glutathione transferase, ferritine (removes metals like iron that promotes oxidative stress), and low molecular weight antioxidants such as vitamin E, vitamin C, vitamin A, uric acid, and bulirubin. However, the production of oxidative species and reduced equivalents is more elevated than defense mechanisms, due to the fact that alcohol inhibits antioxidants [30].