Assessing mercury contamiantion in the Amazon
Methylmercury in humans is often related to the ingestion of methylmercury contaminated fish.
Mainly two disasters, the Minimata and Iraqi incident, have shown that human health risks are associated
with methylmercury ingestion. These two disasters and more recent studies will be discussed before
concentrating on the possible adverse human health effects in the Amazon due to ingestion of methylmercury
contaminated fish. However, some important toxic effects of methylmercury will be discussed first.
Methylmercury is usually ingested and 95% of the ingested methylmercury is absorbed in the gastrointestinal
tract. Methylmercury distributes readily to all tissues, including the brain and fetus, after absorption from
the gastrointestinal tract. The uniform tissue distribution is due to methylmercury's ability to cross diffusion
barriers and penetrate all membranes without difficulty. Although distribution is generally uniform, the highest
levels are found in the kidney. It is believed that methylmercury is transformed to inorganic mercury in cells
of must tissues, including the brain.
The fecal (bilary) pathway is the predominant excretory route for methylmercury. In humans, nearly all of the
mercury in the feces after organic administration is of the inorganic form. Methylmercury is secreted in the
bile and can be reabsorbed in the intestine.
The toxicity of methylmercury is partly related to its ability to diffuse across cell membranes and partly due
to its high affinity for thiol groups (SH-).
Methylmercury is thought to cross the blood brain barrier by binding to L-cysteine complexes in the blood.
The Methylmercury-L-cysteine complex is then transported into the brain via the methionine uptake mechanism,
which is a neutral amino acid carrier (USDHH, 1994). The developing brain undergoes a complex series of
proliferation, differentiation and migration of neurons and glia. It is thought that methylmercury disrupts
these processes by binding to tubilin-SH, causing the impairment of spindle function during cell division.
One should also bear in mind that the binding of mercury to thiol groups might also lead to the dysfunction
of enzymes and proteins through structural changes.
Apart from the neurotoxic effect of methylmercury on human populations, other toxic effects have been reported.
In Greenland it was shown that the frequency of sister-chromatid exchanges, in Eskimos, increased with
increasing blood mercury levels (Wulf et al., 1986). Recently, a study from the Amazon region showed significant
cytotoxic effects in a riverine population exposed to methylmercury through fish ingestion (Amorim et al., 2000).
The mitotic index in peripheral lymphocytes declined with increasing mercury levels. Furthermore, the frequency
of polyploides and chromatid breaks in lymphocytes increased with increasing mercury levels. These findings
suggest that spindle function was disrupted during mitosis. Methylmercury have also been shown to result in
T-cell apoptosis by depleting thiol reserves, which predisposes cells to generate more reactive oxygen species
and at the same time activates death-signalling pathways (Shenker and Shapiro, 1998). Further studies by Shenker
and Shapiro (1999) lead them to propose that the target organelle for methylmercury is the mitochondrion and
confirmed that induction of oxidative stress leads to activation of death-signaling pathways. The above findings
indicate that mercury has a common mechanism of action, which is the disruption of spindle function. Methylmercury
may be regarded as neurotoxic, genotoxic, and immunotoxic. However, only the neurotoxic aspect of methylmercury
will receive further attention.
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