Is Mercury a carcinogen? What is its mechanism of action? A hypothesis beyond genotoxic effects, beyond inhibition of intercellular communication, through epigenetic effects.

We studied mercury toxicity and, in particular, we evaluated that it inhibited the intercellular communication via gap junctions; the latter might explain its carcinogen effect. It is known that a promoter effect occurs by the inhibition of intercellular communication. However, this mechanism cannot, alone, permit to classify mercury as carcinogen. We retain that the increment of reactive oxygen species is associated with the inhibition of the pro-inflammatory cytokines and it may tamper the immune system defences: checkmate the whole organism. Summing up our studies, we propose that the carcinogenic effect of mercury might ensue from: 1) inhibition of gap junctions-mediated intercellular communication linked to increased production of reactive oxygen species [6]; 2) reduction of the pro-inflammatory interleukins IL1 Beta and TNF alpha causing alteration of the earlier immune response [7]. These two mercury-induced key events might act synergically to turn a group of proliferating cells in a war machine highly capable of invading the host tissues. May we call all that as epigenetic effects? If all depends on genes, and the genes can be expressed or not expressed and these events depend on environment, then Mercury is an evident example of epigenetic carcinogen. We would like to conclude with a question “What’s beyond the epigenetic effect?”