Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca(2+) and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain). 2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g., crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation. 3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized. (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetylcholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium. (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume. 4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in teh interalveolar portions of rat's lungs. 5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na+, K+ and Mg(2+) ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium. 6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced. 7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3beta-hydroxysteroid transferase and 17 beta-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals. 790 Sep 59

Occupation and industry codes on death certificates from 23 states for 1984-1988 were used to evaluate mortality risks among white and nonwhite, male and female farmers. Proportionate mortality and proportionate cancer mortality ratios were calculated using deaths among nonfarmers from the same states to generate expected numbers. Among farmers there were 119,648 deaths among white men, 2,400 among white women, 11,446 among nonwhite men, and 2,066 among nonwhite women. Deficits occurred in all race-sex groups for infective and parasitic diseases, all cancer combined, lung cancer, liver cancer, diseases of the nervous system, multiple sclerosis, hypertension, and emphysema. As reported in other studies, white male farmers had excesses of cancer of the lymphatic and hematopoietic system, lip, eye, brain, and prostate. Excesses of cancers of the pancreas, kidney, bone, and thyroid were new findings. Regional patterns were evident, particularly among white men. Significant excesses for accidents, vascular lesions of the central nervous system (CNS), and cancers of the prostate tended to occur in most geographic regions, while excesses for mechanical suffocation, non-Hodgkin's lymphoma, and cancers of the lip, brain, and the lymphatic and hematopoietic system were limited to the Central states. Increases among nonwhite men were similar to those in white men for some causes of death (vascular lesions of the CNS and cancers of the pancreas and prostate), but were absent for others (lymphatic and hematopoietic system, lip, eye, kidney, and brain). Women (white and nonwhite) had excesses for vascular lesions of the CNS, disease of the genitourinary system (white women only), and cancers of the stomach and cervix (nonwhite women only). Cancer of the buccal cavity and pharynx was slightly elevated among women, and white women had nonsignificant excesses of multiple myeloma and leukemia. Excesses for leukemia and non-Hodgkin's lymphoma occurred among white men and women, but not among nonwhites. Excesses for several types of accidental deaths were seen among all race-sex groups.
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PMID:Cancer and other causes of death among male and female farmers from twenty-three states. 850 51