[Effect of glutamic acid on enzyme activity in the rat liver in fluorine poisoning].
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Animals are constantly exposed to a wide variety of foreign chemicals, many of which are potentially toxic and some of which result in the clinical poisonings. Pesticides are applied on or around animals for the control of insects and rodents. These chemicals may be placed in areas without regard for accessibility to household pets and domestic livestock. Insecticides, herbicides, and fungicides are routinely and haphazardly applied to animal and environmental surfaces alike with apparent disregard for differences in absorptive capability. Fortunately, newer herbicides and fungicides are relatively nonhazardous. Drugs are considered to have therapeutic effects, but the lay and professional person's disregard for species differences and variations in recommended dosages can result in poisonings. Adverse reactions may be misnomers for errors in judgment. Failure to provide satisfactory storage facilities for animal feeds and the improper preservation and handling of feedstuffs allow the growth and development of a variety of mycotoxins. Ignorance on the part of animal owners and livestockmen can result in a number of unusual and sometimes fatal clinical syndromes. The dependence of domestic animals and livestock upon their owners for the total environment makes these animals extremely susceptible to environmental pollutants. Exposure to noxious gases, irritating and hazardous industrial materials and wastes, water contaminants, and casually discarded compounds of our own use can and frequently do result in animal illnesses and death. Persons responsible for animals may be unaware of the potential hazard or lack good judgment in the use of these chemicals. Forceful and continuing education for the safe and sensible use of all foreign compounds on and around domestic animals and livestock is needed. Persons handling and applying these materials must recognize their responsibility, not only to themselves but also to their neighbors and the animals in their care.
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It is stated that fluoride intoxication promotes a sharp intensification of the peroxidation processes in the parodontium tissues. It is caused by a respirator explosion of neutrophils, a decrease in activity of antioxidant system enzymes, thus leading to disturbances of microcirculation and blood coagulation, ischemia development. The last factor can retard the enzymatic oxidation in a cell due to hypoxia, injures lysosomal membranes promoting partial autolysis of parodontium tissues, cell structures, intercellular substance. The interaction of blood with destructive elements of cells and collagen favours the development of trombohemorrhagic reactions in the parodontium tissues. A generalized damage of parodontium arises which intensifies under the effect of any other pathogenetic factors.
Thirty seven female patients with osteoporosis underwent iliac bone biopsy after 10 to 23 months of continuous or discontinuous treatment with sodium fluoride, calcium, and vitamin D. Microradiographs of the biopsies from 13 patients showed one or--more often--several of the characteristic appearances of bone fluorosis: defects in periosteocytic mineralization, unmineralized strips inside the trabeculae of spongy bone, construction of fibrous bone, hypercalcified periosteal apposition. The occurrence of these microradiographic signs of fluorosis does not seem to be linked either to the age of the patients, to the interval elapsed since ovarian function ceased, or to the degree of bone remodelling at the time that treatment was started. Moreover, none of these patients showed signs of even moderate renal insufficiency. Should the development of this fluorosis, which is most frequently clinically asymptomatic, be considered as a condition or as a factor in therapeutic efficacy? Or are the effects detrimental and therefore to be avoided by a reduction in dosage or a change in therapeutic methods?
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