Birds pesticide metabolism

We must always recognize that pesticide metabolism studies cannot be considered as an end in themselves but rather, they are a means toward an end. For the ultimate value of a metabolism study, be it in microorganisms, plants, birds, laboratory mammals, or v atever, is its yield of data valuable toward further assessment of the toxicological significance of the pesticide in question to lower organisms (i.e., its environmental impact) or, more importantly, to assess toxicological significance to man himself. 

Birds rapidly and efficiently metabolize fenvalerate by hydrolytic cleavage of the ester bond followed by extensive hydrox-ylation of the acid moiety at the carbon adjacent to the carboxyl group, the methyl group, or both. Major metabolites identified in liver preparations were 2-(4-chlorophenyl)-3-methylbut5Tic acid, 4-hydroxyfenvalerate, 3-phenoxybenzaldehyde, and 3-phenoxybenzoic acid. Liver microsomal drug-metabolizing enzymes usually play an important role in pesticide metabolism however, fenvalerate and other synthetic pyrethroids are very weak inducers of avian microsomal enzymes. Birds are more resistant to fenvalerate than are... 

Because oceans serve as a sink for chlorinated pesticides and CACs, marine mammals and piscivorous birds are consuming relatively high amounts of these compounds, whereas they have a relatively low capacity for metabolism. As a result, they may constitute the most vulnerable organisms with regard to longterm toxicity.14 Over 90% of the whole body burden of marine mammals may be present in their blubber.14... 

Researchers were also able to establish the link between declines of other predatory species such as the European sparrowhawk and the use of organo-chlorine pesticides other than DDT. For instance, the cyclodiene insecticides aldrin, dieldrin, and he-ptachlor used as seed treatments caused massive mortality of both seed-eating species and their predators. All of the insecticides had the following points in common they were highly soluble in fats and refractory to metabolism. The impacts on the predatory species typically take place in periods of food stress when fat soluble residues are released from fat stores and returned into general circulation. In a food-stressed individual, the brain remains as the most lipid rich tissue and this is where contaminants move to. Toxicity results when threshold values in brain tissue are exceeded. At sublethal levels, documented effects of cyclodiene insecticides in birds have included changes in their reproductive, social, and avoidance behaviors. 

Once OPs enter the body, they are mainly metabolized in the liver, gastrointestinal tract, malpighian tubulc.s, and body fat by mixed function oxida.ses, which further increase their toxicity. Oxidative desulfuration of OPs leads to maximum anticholincstera,se activity. To consider the possible toxic effect of OPs, it is necessary to take into account the type of chemical and the species in question because there are wide differences. For example, in vertebrates, after one. single exposure to OP pesticides the recovery time from the amicholincsicrase effecl-s ranges from I to 3 weeks, whereas only approximately 1 day is necessary to recover from exposure to a CM pesticide. Birds and mammals have similar metabolic responses to anticholinesterase pesticides. However, birds tend to be more sensitive to their toxic action, probably due to lower levels of metabolizing enzymes. 

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