Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytochemical changes were studied in leukocytes in peripheral blood smears from rabbits chronically exposed to mercury vapor. Experimental animals were exposed in a toxicologic chamber to air containing metallic mercury in concentrations of 2.0-2.5 mg/m3 for 3 hours daily over 12 weeks. In the poisoned rabbits, as compared with controls, alkaline phosphatase activity was depressed in granulocytes, and lactate dehydrogenase activity in granulocytes and lymphocytes. The activities of acid phosphatase, arylsulphatase, 5'-nucleotidase, the color reaction with Sudan black B and the p.a.S. reaction were not affected.
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PMID:Cytochemical abnormalities of the leukocytes of peripheral blood of rabbits in chronic experimental intoxication with mercuric vapors. 122 12

The aim of the present investigation was to evaluate the effect of a subchronic treatment (30 days/30 doses) with subcutaneous injections (0.1 mg/kg) of HgCl2 on NTPDase (E.C. 3.6.1.5), 5'-nucleotidase (E.C 3.1.3.5) and acetylcholinesterase (AChE, E.C. 3.1.1.7) activities in brain from adult rats. NTPDase and 5'-nucleotidase were measured in cortical synaptosomal fraction and AChE was measured in the homogenate of cerebral cortex and hippocampus. After the subchronic treatment (30 days), NTPDase activity was enhanced approximately 35% (p < 0.05) with ATP and ADP as substrates and no difference was observed in 5'-nucleotidase activity (AMP hydrolysis). In addition, AChE activity was enhanced in the cerebral cortex (22%, p < 0.05) and hippocampus (26%, p < 0.05) after the subchronic treatment. Mercury deposited in brain was measured by cold vapor (atomic absorption spectrometry) and no difference between the control and the subchronically treated group was observed. Here we showed for the first time that exposure to low levels of Hg2+, which resembles occupational exposure to low levels of mercury, caused a marked increase in NTPDase and AChE activities. The relationship of these alterations with the neurotoxicity of inorganic mercury deserves further studies.
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PMID:Effect of subchronic treatment with mercury chloride on NTPDase, 5'-nucleotidase and acetylcholinesterase from cerebral cortex of rats. 1513 88

Neurotransmission can be affected by exposure to heavy metals, such as mercury and lead. ATP is a signaling molecule that can be metabolized by a group of enzymes called ecto-nucleotidases. Here we investigated the effects of mercury chloride (HgCl(2)) and lead acetate (Pb(CH(3)COO)(2)) on NTPDase (nucleoside triphosphate diphosphohydrolase) and ecto-5'-nucleotidase activities in zebrafish brain membranes. In vitro exposure to HgCl(2) decreased ATP and ADP hydrolysis in an uncompetitive mechanism and AMP hydrolysis in a non-competitive manner. Pb(CH(3)COO)(2) inhibited ATP hydrolysis in an uncompetitive manner, but not ADP and AMP hydrolysis. In vivo exposure of zebrafish to HgCl(2) or Pb(CH(3)COO)(2) (20mug/L, during 24, 96h and 30 days) caused differential effects on nucleotide hydrolysis. HgCl(2), during 96h, inhibited the hydrolysis of ATP, ADP and AMP. After 30 days of exposure to HgCl(2), ATP hydrolysis returned to the control levels, ADP hydrolysis was strongly increased and AMP hydrolysis remained inhibited. Exposure to Pb(CH(3)COO)(2) during 96h caused a significant decrease only on ATP hydrolysis. After 30 days, Pb(CH(3)COO)(2) promoted the inhibition of ATP, ADP and AMP hydrolysis. Semi-quantitative RT-PCR analysis showed no changes in the expression of NTPDase1 and 5'-nucleotidase, following 30 days of exposure to both metals. This study demonstrated that Hg(2+) and Pb(2+) affect the ecto-nucleotidase activities, an important enzymatic pathway for the control of purinergic signaling.
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PMID:Exposure to Hg2+ and Pb2+ changes NTPDase and ecto-5'-nucleotidase activities in central nervous system of zebrafish (Danio rerio). 1693 Jul 98

The effectiveness of the antioxidant thiol, N-acetylcysteine (NAC), in enhancing methylmercury (CH3HgCl) excretion and its utility as a possible antidote in CH3HgCl poisoning has been reported. NAC, however, has been reported to be ineffective in accelerating excretion of divalent toxic metals, including inorganic mercury, Hg2+. In this study, we evaluated the possible protective effect of short-term pretreatment with NAC against mercuric chloride (HgCl2) toxicity in rat model. This is aimed at determining its chemopreventive or prophylactic benefit in situations of high risk exposure (occupational/industrial) to mercury. Rats were divided into three treatment groups. Group I received saline (10 ml/kg) and served as control. Group II received HgCl2 (5mg/kg) and group III received NAC (10mg/kg) plus (5mg/kg). All administration was via intraperitoneal (i.p.) injection. Saline and NAC were administered for 5days and HgCl2 was administered to rats in groups II and III on the 5th day. Animals were sacrificed 24 hours after HgCl2 injection and samples obtained for biochemical evaluation. Results revealed that single i.p. injection of HgCl2 induced significant renal oxidative damage resulting in significant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST), depletion of reduced glutathione (GSH) and increase in malondialdehyde (MDA) levels in these rats. The activities of glucose-6-phosphatase (G6Pase) and 5'-nucleotidase (5'-NTD) (markers of microsomal damage) also decreased in these HgCl2 treated rats. The oxidative damage induced by HgCl2 led to significant alterations in renal histology and caused functional impairment (indicated by elevated blood urea nitrogen (BUN) and serum creatinine) in these rats. NAC was effective in attenuating the oxidative damage, functional impairments and histopathological changes that characterized HgCl2 intoxication in this study. Renal antioxidant defense system was re-enforced by NAC, leading to increase in the activities of SOD, CAT, GST and decreases in GSH depletion and MDA level. Our results therefore reveal the ameliorative effect of NAC pretreatment against HgCl2 toxicity in vivo, thus, suggesting its usefulness as a possible chemoprophylactic agent during occupational or industrial exposure to inorganic mercury.
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PMID:N-acetylcysteine pretreatment ameliorates mercuric chloride-induced oxidative renal damage in rats. 2241 58