Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In last decade it was suggested that the metabolism and toxicity of some xenobiotics may be modified by several compounds that alter the activities of microsomal oxidative and conjugating enzymes. In present study the effect of ethanol on benzene metabolism and benzene-induced hemotoxicity in pregnant rats was investigated. Pregnant female Wistar rats were exposed to benzene vapors for 6 hr/day from Days 8 through 15 of gestation at concentrations of 1500 and 3000 mg/m3 or combination ethanol and benzene at the same concentrations. Ethanol was administered intragastrically at a dose of 2.5 g/kg directly before exposure to benzene or 18 hrs before. An air-exposed or ethanol treated control rats were also studied. Before, during and after exposure blood samples for leukocyte and lymphocyte counts were obtained and urine for free phenol and conjugated phenol determinations was collected. Exposure to benzene alone decreased the maternal body weight and reduced leukocyte and lymphocyte counts in peripheral blood. Ethanol administered directly before exposure to benzene in principle had no effect on the metabolism and toxicity of benzene. It reduced the conversion of benzene to free and conjugated phenol, and protected animals from reduction of body weight and lymphopenia when was given 18 hrs before. Obtained results indicate that the early phases of benzene metabolism and its toxicity may be modified by ethanol.
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PMID:[Modification of metabolism and toxicity of benzene by ethanol in pregnant rats]. 184 23

Polybrominated diphenyl ethers (PBDEs) are persistent, bioaccumulative, organohalogen compounds that are increasing exponentially in the Great Lakes (Canada/USA) biota. The present study was undertaken to examine the immunological effects of a commercial PBDE mixture in ranch mink (Mustela vison). Twenty-week-old mink (n = 10 mink/group) were exposed to 0, 1, 5, or 10 ppm of DE-71 through their diet for eight weeks. The phytohemagglutinin-induced cutaneous reaction, and antibodies specific to keyhole limpet hemocyanin conjugated to dinitrophenol were measured. Liver microsomal ethoxyresorufin-O-deethylase (EROD) activity also was measured. Organs were weighed and spleens were examined histologically. No differences were found in the PHA-induced skin response in exposed mink; mink in the two highest treatments exhibited significant increases in antibody production over control mink. Systemic toxicity was apparent; significant body weight reductions were found in mink exposed to 5 and 10 ppm of DE-71. Exposed mink had significantly larger relative spleen, adrenal, and liver masses than control mink. Spleens of mink exposed to 10 ppm of DE-71 had significantly increased germinal center development and incidence of B-cell hyperplasia. The activity of EROD was induced in all treated mink relative to controls and was positively associated with the liver somatic index. Hematocrit in mink from the two highest exposure groups was significantly lower than control mink. Percentage neutrophils increased and percentage lymphocytes decreased significantly in mink from the higher two dosage groups. Our findings have direct relevance to wild mink in the Great Lakes ecosystem, because mink are top predators of the aquatic food web, providing evidence for the vulnerability of this species to the effects of environmental PBDE mixtures.
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PMID:Immunotoxicity of the commercial polybrominated diphenyl ether mixture DE-71 in ranch mink (Mustela vison). 1752 Nov 47