Dithiolthiones, particularly 1,2-dithiole-3-thione and its derivatives (such as oltipraz), have been investigated for their potential hepatoprotective effects, including in the context of fatty liver disease (non-alcoholic fatty liver disease, NAFLD). The scientific rationale lies in their ability to induce phase II detoxification enzymes via activation of the Nrf2 (nuclear factor erythroid 2–related factor 2) pathway, which upregulates antioxidant defenses in the liver and may reduce oxidative stress—a key factor in the progression of fatty liver disease to steatohepatitis and fibrosis.

Several animal studies have shown that dithiolthiones can attenuate hepatic steatosis, reduce markers of liver injury, and improve antioxidant status. For example, oltipraz has been demonstrated in rodent models to decrease hepatic lipid accumulation and suppress inflammation associated with NAFLD. However, clinical evidence in humans is very limited. Only a few early-phase clinical trials have evaluated oltipraz in liver diseases, with some suggestion of biochemical improvement, but robust, large-scale trials specifically in NAFLD/NASH are lacking.

In summary, while there is a plausible mechanism and supporting preclinical data, the evidence base for dithiolthiones in the treatment of fatty liver disease in humans is weak and insufficient for clinical recommendation at this time.