Enzyme reactions cellular toxicity, mechanisms

Adults require 1-2 mg of copper per day, and eliminate excess copper in bile and feces. Most plasma copper is present in ceruloplasmin. In Wilson s disease, the diminished availability of ceruloplasmin interferes with the function of enzymes that rely on ceruloplasmin as a copper donor (e.g. cytochrome oxidase, tyrosinase and superoxide dismutase). In addition, loss of copper-binding capacity in the serum leads to copper deposition in liver, brain and other organs, resulting in tissue damage. The mechanisms of toxicity are not fully understood, but may involve the formation of hydroxyl radicals via the Fenton reaction, which, in turn initiates a cascade of cellular cytotoxic events, including mitochondrial dysfunction, lipid peroxidation, disruption of calcium ion homeostasis, and cell death. 

Surfactant Effects on Microbial Membranes and Proteins. Two major factors in the consideration of surfactant toxicity or inhibition of microbial processes are the disruption of cellular membranes b) interaction with lipid structural components and reaction of the surfactant with the enzymes and other proteins essential to the proper functioning of the bacterial cell (61). The basic structural unit of virtually all biological membranes is the phospholipid bilayer (62, 63). Phospholipids are amphiphilic and resemble the simpler nonbiological molecules of commercially available surfactants (i.e., they contain a strongly hydrophilic head group, whereas two hydrocarbon chains constitute their hydrophobic moieties). Phospholipid molecules form micellar double layers. Biological membranes also contain membrane-associated proteins that may be involved in transport mechanisms across cell membranes. 

One theory of the mechanism of acute selenium toxicity concerns inactivation of the sulfhydryl enzymes necessary for the oxidative reactions in cellular respiration (Lombeck et al. 1987 Mack 1990 Shamberger 1981). Acute toxic effects, such as pulmonary edema, can result in respiratory failure and death. The lung, however, does not appear to be a target organ at levels of exposure less than the occupational permissible exposure limits (PELs) or threshold limit values (TLV). 

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