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Carbon disulfide (CS(2)) is a severe environmental pollutant. There is consensus that CS(2) is a liver carcinogen, however, the mechanism(s) of CS(2)-induced liver cancer is not well understood. The ability of CS(2) to induce oxidative stress has been well documented; however, there is also evidence that CS(2) has the ability to induce apoptosis as well as protect cells from oxidative stress. Studies using transgenic mice have shown that glutathione (GSH) depletion is an important factor in CS(2)-induced toxicity. In the presence of GSH, CS(2) can be detoxified primarily by the tripeptide glutathione-S-transferase (GST). It is not known how CS(2) modulates GST activity to result in the predominant detoxification of this compound. CS(2) has also been shown to induce a small amount of non-electrophile-based GST activity. The induction of other forms of GST activity, including that mediated by quinone-reductase, may play a role in CS(2)-induced toxicity. Under certain conditions, CS(2) may be able to induce GSH biosynthesis. A number of studies have shown that CS(2) is able to induce CYP enzymes and, as a result, CS(2) can enhance the bioactivation and biotransformation of benzo(a)pyrene (BaP). Recent studies have shown that CS(2) can protect against BaP-induced toxicity in multiple cell types. The ability of CS(2) to protect against BaP toxicity was shown to be mediated by the transcription factor Nrf2 and by inhibition of CYP1A2 activity. In addition, CS(2) prevented BaP-induced increases in both the expression and activity of drug-metabolizing enzymes, including CYP1A2 and GST. As a result, CS(2) can protect against a variety of toxic compounds in addition to BaP. The ability of CS(2) to protect against toxic compounds may have important implications in human health. Studies with the overexpressing GSTP
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