Target organ toxicity in marine and freshwater teleosts. / by W.H. Benson, Daniel Schlenk

By W.H. Benson, Daniel Schlenk

Addressing the varied gaps in present details, aim Organ Toxicology in Marine and Freshwater Teleosts is a necessary source for researchers and pros in aquatic toxicology and environmental chance evaluate. the entire chapters are written through researchers who're across the world acknowledged for his or her paintings in mechanistic features of aquatic toxicology. every one bankruptcy makes a speciality of a selected aim organ or Read more...

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Addressing the varied gaps in present details, a necessary source for researchers and pros in aquatic toxicology and environmental chance assessment. Read more...

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Extra resources for Target organ toxicity in marine and freshwater teleosts. / Volume 1, Organs

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The former, at least, appears to be associated with a marked hyperplasia of chloride cells. , 1989; Playle and Wood, 1989b, 1991; Wood, 1989; Spry and Wiener, 1991; Heath, 1995; Poleo, 1995; Brown and Waring, 1996; Sparling and Lowe, 1996; Wilson, 1996). It is the third most abundant element in the earth’s crust and is highly soluble at low pH, so most naturally acidified freshwaters contain substantial amounts of aluminum, which may pose a larger threat to the fish than the acidity itself. Aluminum is a specific surfaceactive toxicant at the gills; indeed, its ability to penetrate into the bloodstream is negligible.

The latter would be driven by the Na+ gradient, and therefore indirectly energized by the basolateral Na+,K+-ATPase. Intracellular Ca2+ activities are extremely low (submicromolar) because of the presence of Ca2+ binding proteins. Thus, the basolateral exit is active, whereas the apical entry is passive, along the electrochemical gradient. , 1998). Unidirectional Ca2+ flux rates are low, generally less than 10 percent of Na+or Cl-flux rates. Marine teleost fish maintain internal osmolalities only slightly higher than those of freshwater fish (320–400 mosmol) despite high external osmolality (1050 mosmol in 100 percent seawater) which continually extracts water from the fish, mainly across the gills.

Handling, crowding, hypoxia, low social rank). This latter conclusion emphasizes the extreme caution that must be exercised when holding and killing fish for gill morphology in toxicologic studies and the lack of value in sampling fish close to or at death for gill structural indices. Most lesions are independent of temperature, and, in a few cases, physiologic perturbation and death may occur in the absence of obvious gill pathology. Thus, structural changes in the gills, although obviously indicative of damage, are not a good diagnostic tool for the toxicant which is the causative agent of that damage, for its concentration or exposure duration, or for its key toxic mechanism of action at a physiologic level.

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