Superoxide Dismutase (SOD) is an endogenous antioxidant enzyme that catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide, playing a crucial role in cellular defense against oxidative stress. Hepatitis, particularly viral and alcoholic hepatitis, is characterized by increased oxidative stress and inflammation in liver tissues. Several preclinical studies (in vitro and animal models) have explored the potential of SOD in ameliorating liver damage caused by oxidative stress. These studies indicate that SOD administration or upregulation can reduce markers of oxidative damage, inflammation, and liver enzyme leakage, suggesting a hepatoprotective effect.

However, direct clinical evidence in humans is limited. A few small-scale clinical trials and pilot studies have investigated SOD or SOD mimetics in patients with liver disease, including hepatitis, with some reporting improvements in oxidative stress markers or biochemical parameters. Nevertheless, these studies are often limited by small sample sizes, lack of controls, and methodological weaknesses. There is no large-scale, high-quality randomized controlled trial confirming SOD's efficacy as a treatment for hepatitis in humans.

In summary, while there is a plausible scientific rationale and promising preclinical evidence supporting the use of SOD in hepatitis, its clinical application is not well established. The current evidence base rates as low to moderate (2/5), with further robust human studies needed to validate its therapeutic role in hepatitis.