ISBN-10: 0203361407
ISBN-13: 9780203361405
RETAILESQUE
Addressing the various gaps in present details, aim Organ Toxicology in Marine and Freshwater Teleosts is an important source for researchers and execs in aquatic toxicology and environmental chance evaluate. the entire chapters are written via researchers who're across the world known for his or her paintings in mechanistic facets of aquatic toxicology. each one bankruptcy makes a speciality of a particular objective organ or physiological method and describes how quite a few brokers disrupt the traditional physiological process and methods. This quantity is dedicated to precise organs with assurance of the gill, kidney, epidermis, liver and intestine. The significant other quantity, structures, presents assurance of poisonous results within the valuable apprehensive, immune, neurobehavioural and reproductive structures in addition to describing common mechanisms of toxicity.
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Extra resources for Target Organ Toxicity in Marine and Freshwater Teleosts: Organs
Example text
High levels of most toxicants generally cause an initial increase in flux rates of respiratory gases across the gills. These are associated with increased consumption of O2 and production of CO2 and ammonia at the systemic tissues as a result of excitement and escape responses. Increased gas exchange is facilitated by the rapid mobilization (within seconds) of catecholamines into the plasma from chromaffin tissue and increased sympathetic nervous activity. These agents dilate the gills, open up more respiratory lamellae, favor the arterioarterial pathway and reduce flow in the arteriovenous pathway, increase blood pressure and cardiac output, and generally shunt blood flow through pathways more favorable for gas exchange in lamellae.
E. levels well above the 96-h LC50 value). As these responses are of limited mechanistic relevance, they will be only briefly summarized here, based on a synthesis of several sources (Hughes, 1976; Satchell, 1984; Evans, 1987; Barton and Iwama, 1991; Wendelaar Bonga and Lock, 1992; Heath, 1995; McDonald and Milligan, 1997; Wendelaar Bonga, 1997). High levels of most toxicants generally cause an initial increase in flux rates of respiratory gases across the gills. These are associated with increased consumption of O2 and production of CO2 and ammonia at the systemic tissues as a result of excitement and escape responses.
Indeed, there is considerable circumstantial evidence (summarized by Wendelaar Bonga, 1997) that the whole cell cycle of mitosis, maturation, senescence, and death is accelerated during sublethal toxicant exposure. Obviously, proliferation of ion-transporting cells should help increase active electrolyte transport, and the general thickening of the epithelia and increased mucous cell activity should help reduce diffusive ion permeability. However, ion transport rates or activities of key transport enzymes may not be as high as indicated by the number of chloride cells because a greater percentage of them may be immature, dying, or otherwise impacted by the toxicant (Wendelaar Bonga and Lock, 1992).