Marie E. Vahter
Abstract
Exposure to arsenic through drinking water
is a major public health problem affecting most countries, although the
situation
is particularly severe in low-income nations. The
health consequences of chronic arsenic exposure include increased risk
for
various forms of cancer and numerous noncancer
effects, including diabetes, skin diseases, chronic cough, and toxic
effects
on liver, kidney, cardiovascular system, and
peripheral and central nervous systems. In recent years increasing
reports of
effects on fetal and child development have
appeared. There seems to be a wide variation in susceptibility to
arsenic toxicity,
which is likely to be related to factors such as
variation in arsenic metabolism, nutrition, host-related defense
mechanisms,
and genetic predisposition. The main mechanisms of
arsenic-nutrition interactions include arsenic-induced oxidative stress,
which requires nutrient-dependent defense systems,
and arsenic metabolism (methylation) via 1-carbon metabolism, which
requires
methyl groups, folic acid, vitamin B-12, and
betaine for the remethylation of homocysteine to methionine. An
efficient first
methylation step in combination with a slow second
methylation step seems to be most critical from a toxicological point of
view. A third mode of arsenic-nutrition interaction
involves epigenetic effects and fetal programming via DNA methylation.
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