This book describes the present state of knowledge regarding the impact of cyanobacteria on health through the use of water. It considers aspects of risk management and details the information needed for protecting drinking water sources and recreational water bodies from the health hazards caused by cyanobacteria and their toxins. It also outlines the state of knowledge regarding the principal considerations in the design of programmes and studies for monitoring water resources and supplies and describes the approaches and procedures used.
The development of this publication was guided by the recommendations of several expert meetings concerning drinking water (Geneva, December 1995; Bad Elster, June
1996) and recreational water (Bad Elster, June 1996; St Helier, May 1997). An expert meeting in Bad Elster, April 1997, critically reviewed the literature concerning the toxicity of cyanotoxins and developed the scope and content of this book. A draft manuscript was reviewed at an editorial meeting in November 1997, and a further draft was
reviewed by the working group responsible for updating the Guidelines for Drinkingwater Quality in March 1998.

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Toxic cyanobacteria in water: a guide to their public health consequences, monitoring and management.

the toxicology of microcystins

This review focuses on the risk assessment associated with human exposure to cyanotoxins, secondary metabolites of an ubiquitous group of photosynthetic procariota. Cyanobacteria occurr especially in eutrophic inland and coastal surface waters, where under favorable conditions they attain high densities and may form blooms and scums. Cyanotoxins can be grouped according to their biological effects into hepatotoxins, neurotoxins, cytotoxins, and toxins with irritating potential, also acting on the gastrointestinal system. The chemical and toxicological properties of the main cyanotoxins, relevant for the evaluation of possible risks for human health, are presented. Humans may be exposed to cyanotoxins via several routes, with the oral one being by far the most important, occurring by ingesting contaminated drinking water, food, some dietary supplements, or water during recreational activities. Acute and short-term toxic effects have been associated in humans with exposure to high levels of cyanotoxins in drinking and bathing waters. However, the chronic exposure to low cyanotoxin levels remains a critical issue. This article identifies the actual risky exposure scenarios, provides toxicologically derived reference values, and discusses open issues and research needs.

Human Health Risk Assessment Related to Cyanotoxins Exposure

Research over the last decade has extended the prevailing view of mitochondria to include functions well beyond the critical bioenergetics role in supplying ATP. It is now recognized that mitochondria play a crucial role in cell signaling events, inter-organelle communication, aging, many diseases, cell proliferation and cell death. Apoptotic signal transmission to the mitochondria results in the efflux of a number of potential apoptotic regulators to the cytosol that trigger caspase activation and lead to cell destruction. Accumulating evidence indicates that the voltagedependent anion channel (VDAC) is involved in this release of proteins via the outer mitochondrial membrane. VDAC in the outer mitochondrial membrane is in a crucial position in the cell, forming the main interface between the mitochondrial and the cellular metabolisms. VDAC has been recognized as a key protein in mitochondria-mediated apoptosis since it is the proposed target for the pro- and anti-apoptotic Bcl2-family of proteins and due to its function in the release of apoptotic proteins located in the inter-membranal space. The diameter of the VDAC pore is only about 2.6-3 nm, which is insufficient for passage of a folded protein like cytochrome c. New work suggests pore formation by homooligomers of VDAC or hetero-oligomers composed of VDAC and pro-apoptotic proteins such as Bax or Bak. This review provides insights into the central role of VDAC in cell life and death and emphasizes its function in the regulation of mitochondria- mediated apoptosis and, thereby, its potential as a rational target for new therapeutics.

The Voltage-Dependent Anion Channel (VDAC): Function in Intracellular Signalling, Cell Life and Cell Death

Microcystins produced by cyanobacteria are potent and specific hepatotoxins; however, the mechanisms of microcystin-induced hepatotoxicity have not been fully elucidated. The induction of free radical formation and mitochondrial alterations are two major events found in microcystin-treated cultured rat hepatocytes. The mitochondrial alterations, i.e. loss of mitochondrial membrane potential and mitochondria permeability transition are now recognized as key steps in apoptosis. The activation of calpain and Ca2+/calmodulin-dependent protein kinase II is believed to be critical in the microcystin-induced apoptotic process.

C.M McDermott

Papers

The cyanobacterial toxin, microcystin-LR, can induce apoptosis in a variety of cell types

Detection of cyanobacterial toxins (microcystins) in waters of northeastern Wisconsin by a new immunoassay technique.