In Vitro Toxicity of Methyl Mercury to Fathead Minnow Cells

Effect of cortisol treatment and/or sublethal copper exposure on copper uptake and heat shock protein levels in common carp, Cyprinus carpio

“…The absence of a clear relationship between the HSP response and Cu accumulation seems to indicate that the HSP response is probably more related to secondary effects of Cu toxicity than the direct action of this metal. It has been suggested from experiments with the isopod Oniscus asellus exposed to high cadmium levels and CCL‐42 (American Type Culture Collection, Rockville, MD, USA) fathead minnow cells exposed to levels of methyl mercury that the decrease of the HSP response may be related to the loss of physiological compensation [32,33]. However, the concentrations used in these studies resulted in cell mortality within 96 h, while exposure concentrations in this experiment were only a fraction of the 96‐h LC50 value of 9 μM [34].…”

Feeding mice with diets containing mercury-contaminated fish flesh from French Guiana: a model for the mercurial intoxication of the Wayana Amerindians

“…When addressing the question as to whether mouse is a pertinent model for the mercurial intoxication of the Wayana Amerindians, a good criterion consists in a comparison of the mercury concentrations impairing cell life, i.e. resulting in cell death or limited cell viability, among various cell lines from different origins (Table 9 ) including bacteria [ 45 ], yeast [ 46 ], clam [ 47 ], worm [ 48 ], mosquito [ 49 ], chicken [ 50 ], fish [ 51 ], rabbit [ 52 ], rat [ 31 , 53 , 54 ], mouse [ 32 , 53 , 55 , 56 ], and man [ 57 - 59 ]. Remarkably, most of these values are ranging between 1 to 10 μM methylmercury whatever the considered organism, from bacteria to man, and for different cell types.…”

A proteome analysis of the cadmium and mercury response in Corynebacterium glutamicum

“…Heat-shock proteins are molecular chaperones that assist abnormal proteins accumulating under stress conditions to regain their proper folding or assist their proteolytic degradation [38]. Surprisingly the cells did not induce heat-shock proteins after the exposure to Hg 21 , although these proteins were expressed in rat kidney and Fathead Minnow cells upon Hg 21 stress [12,13]. Most of chaperones and proteases, in addition to their protective functions, it may help to reorchestrate the cell metabolism to the needs of the oxidative stress response [38].…”

“…The authors found the induction of these proteins is important for cells in order to counteract the toxic effect of mercury [12]. Devlin and Clary [13] exposed Fathead Minnow cells to MeHg; they found the production of hsp70 was increased under MeHg exposure. Despite of extensive research, the toxic mechanism remains poorly understood and further research in this area is needed.…”