Organometallic Compounds - Organic Pollutants: An Ecotoxicological Perspective - page 169

biochemical effects arising from mercury poisoning, for many proteins depend on
free -SH groups for their normal function.
A prime target for methyl and other organic forms of mercury is the nervous
system, especially the central nervous system (CNS). Here lies an important distinc-
tion between the toxicity of organic and inorganic mercury salts. Although inorganic
forms of mercury can also bind to -SH groups, they cannot readily cross the blood-
brain barrier, and so show less tendency than lipophilic organic mercury to reach the
CNS and cause toxic effects there. Rather, inorganic mercury expresses its toxicity
elsewhere (e.g., in the kidney and on cardiac function). Methyl mercury can cause
extensive brain damage, including degeneration of small sensory neurons of the
cerebral cortex. At the biochemical level, it binds to cysteine groups of acetylcholine
receptors (Crosby 1998) and also inhibits Na + /K + ATP-ase (Clarkson 1987).
With growing interest in the sublethal effects of methyl mercury, evidence has
come to light of changes in the concentration of neurochemical receptors of the
brain during the early stages of poisoning. Studies with mink dosed in captivity
have shown that environmentally realistic levels of methyl mercury can cause (1) an
increase in the concentration of brain muscarinic receptors for acetylcholine, and (2)
a decrease in the concentration of N -methyl-d-aspartic acid glutamate receptors for
glutamate (Basu et al. 2006, and Scheuhammer and Sandheinrich 2008). In the next
section, field studies will be discussed, which have looked for evidence of effects of
this kind in wild mammals and birds.
BOX 8.1 tHe mInamata InCIdent
The neurotoxicity of organomercury was graphically illustrated in an envi-
ronmental disaster at Minamata Bay in Japan during the late 1950s and early
1960s. Release of both organic and inorganic mercury from a factory led to
the appearance of high levels of methyl mercury in the neighboring marine
ecosystem. Levels were high enough in fish to cause lethal intoxication of local
people for whom fish was the main protein source. People died as a conse-
quence of brain damage caused by methyl mercury. The victims had brain Hg
levels in excess of 50 ppm.
In mammals, methyl mercury toxicity is mainly manifest as damage to the CNS
with associated behavioral effects (Wolfe et al. 1998). Initially, animals become
anorexic and lethargic and, with progression of toxicity, muscle ataxia and visual
impairment are seen. Finally, convulsions occur, which lead to death. In dosing
experiments with mink ( Mustela vison) , dietary levels of methyl mercury of 1.1 ppm
fed over a period of 93 days produced subclinical neurological lesions (Wobeser
et al. 1976), and this has been proposed as a lowest observed adverse effect level
(LOAEL). In another study, otters ( Lutra canadensis ) were dosed with 2, 4, or 8
ppm methyl mercury in the diet (Connor and Nielsen 1981). Anorexia and ataxia
were reported at 2 ppm in two-thirds of individuals; anorexia, ataxia, and neurologi-
cal lesions at 4 ppm; and all the symptoms, leading to death at 8 ppm. The brain
Hg concentrations (ppm per unit wet weight) at dose levels of 2, 4, and 8 ppm were