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Book Review |
Dean, College of Agriculture
California State Polytechnic University, Pomona, CA
Metal Ions in Biological Systems, Vol. 34 Mercury and Its Effects on Environment and Biology, edited by Astrid Sigel and Helmut Sigel. Marcel Dekker, Inc., New York, 1997, 604 pages, $250.
To the extreme credit of Astrid and Helmut Sigel, this series has established the "gold standard" for quality publications on mineral metabolism and the biological roles of metal ions. Over the last 24 years, each publication (34 volumes in all) has attracted the world’s best researchers who have written on the hottest topics in science related to bioinorganic chemistry, biochemistry, biology, and medicine.
The existing volume on mercury and its impact on the environment is of major interest. The 19 chapters clearly identify concerns about mercury and its biologic impact on biogeochemical processes including terrestrial, oceanic and atmospheric environs, and the chemistry and toxicity (poisoning) of mercury as it relates to man, animals and fish.
Mercury (Hg) occurs in nature as ionic and elemental mercury. Natural sources include the weathering of cinnabar (HgS) deposits and volcanic and geothermal emissions. Man-made sources include dental amalgams, pharmaceuticals, cosmetics, the exploitation of geothermal fields, chloralkali plants, and other industrial activities such as manufacture of electrical products and paper and pulp mills. Synthetic organomecurials have been banned for decades. Today, the major source of human exposure to Hg is through the diet from consumption of fish and fish products.
More than 90% of total Hg in muscle tissue of top marine predators is monomethymercury (MMeHg), the most toxic species of Hg. MMeHg crosses cell membranes by passive diffusion beginning with the intestinal wall. Its long half life in biological tissues leads to accumulation of high concentrations at the top of the food chain. Minimal increases in MMeHg content of autotrophic organisms produces an unexpectedly large accumulation of Hg (biomagnification) in carnivores, as the terminal end of the food chain.
The transformation of inorganic Hg to MMeHg by microbial methylation is a result of adaption against Hg toxicity. Enzymatic reduction of Hg+2 to Hg0 and confers high resistance to inorganic mercury salts. This narrow-spectrum of Hg resistance is located in plasmids in the inducible mer operon. The enzyme, mercuric reductase, is codified by the merA gene. Less common, but very important, are the broad-spectrum Hg-resistant bacteria, which cleave the C-Hg bond of organomercurials by the enzyme organomecurial lyase, codified by the merB gene. Other sulphydryl proteins are involved in the control, binding, and transport of Hg. Under anaerobic conditions, Hg toxicity is drastically reduced by organic and inorganic sulfides such as H2S. The latter reacts with Hg+2 and MMeHg to produce the stable HgS and the volatile dimethylmercury (DMeHg). MMeHg is also formed and it accumulates to the top of the food chain. Importantly, bacteria convert toxic forms of Hg to harmless forms to protect themselves and in so doing detoxify the surrounding environment as well.
Recent development of specific methodologies has made it possible to determine the Hg species at the femtomole levels. Analytical determination of Hg+2 and MeHg compounds is essential to delineate some of the problems with identification of the specific mercurial compounds in environmental samples. Ethyl-derivatization in combination with atomic fluorescence spectrophotometry has greatly enhanced identification and analytical quantitation. Interlaboratory agreement is improving which enhances reliability of individual studies; yet, many areas of sample preparation need further analytical work, e.g., extraction from marine plants.
Man has disrupted the natural balance established by earth’s evolution, elevating mercury to very high levels in certain regions of the world. In freshwater ecosystems, both the concentrations and the turnover rates of Hg and MeHg are highly variable due to a variety of environmental factors. The quantitative understanding of the numerous mechanisms needs to be improved to enhance protection of freshwater resources. From the marine environment less studies have been made, yet atmospheric recycling of Hg, air-sea exchange, and its influence on biogeochemical behavior, bioaccumulation and fate of Hg in marine waters are essential to our understanding. Further systematic oceanographic investigations are needed using multidisciplinary approaches to form comprehensive predictive modeling.
Mercury has not been characterized as essential for any biologic reaction. However, it is readily accumulated in the body due to many defense mechanisms. Based on sulphydryl binding inside the cell, mercury is trapped to minimize its general distribution and inhibition of essential biologic processes.
MeHg from the diet is almost completely absorbed following digestion. Distribution to the bloodstream and to other tissues is essentially completed within 4 days, but the maximum accumulation in the brain takes 4 to 6 days. At that point, the brain contains 6% of the total dose of MeHg given. Kidney, liver, lung and striated muscle tend to be relatively high in total mercury, whereas other organs such as heart, pancreas and spleen are relatively low.
The central nervous system (CNS) is the critical target organ in MeHg toxicity. The earliest symptoms of intoxication in adults are non-specific from the CNS including paresthesia and malaise. Subsequently, coordination problems, hearing impairment, and constriction of the visual field. Specific areas of the CNS are damaged, such as the visual cortex of the cerebrum and the granular cells of the cerebellum. The developing brain is particularly sensitive to MeHg and the fetal brain may even be affected even when the mother shows no signs of poisoning—MeHg may inhibit both cell proliferation and migration.
Other research areas presented in the book, included Hg-induced aberrant immune responses. Mercury can produce hypersensitivity reactions, systemic autoimmunity and nephrotic syndrome due to membranous glomerulonephritis. Animal models suggest deposition of immune complexes and complement as a feature of the Hg-induced kidney damage.
Mercury interacts strongly with nucleic acids and proteins. Inorganic mercury ions cause a specific inhibition of brain tubulin binding of GTP, and interacts strongly, yet reversibly, with the N-binding sites of purines and pyrimidines. Whereas, organic mercurial compounds produce irreversible damage to nucleic acids.
Many other areas of bio-toxicology were discussed that would be of interest to the environmentalist, bio-inorganic or biochemistry researcher, or students and teachers. This is the ultimate reference text on mercury.
Received December 1, 1997.
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