Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of mercury on renal lysosomal protein digestion was studied after administration of mercury in vitro and in vivo. Mercuric chloride or methylmercury chloride was added in vitro to lysosomal enzymes isolated from normal rats, and subsequently, digestion experiments were carried out using 125I-labeled lysozyme or cytochrome c as substrate proteins. Both mercury compounds produced a concentration-dependent inhibition of the degradation of the proteins, mercuric chloride being the strongest inhibitor. Mercuric chloride was also administered to rats in vivo for 5 to 8 months. Renal lysosomal enzymes from these animals also had a decreased ability to digest for the two substrate proteins. Furthermore, the digestion of lysozyme intravenously injected into mercury-intoxicated rats was decreased in renal cortical slices incubated in vitro. Electron microscope autoradiography showed that intravenously injected labeled lysozyme was located primarily over lysosomes in proximal tubule cells 1 hour after injection in both control animals and mercury-intoxicated rats. These results suggest a decreased catabolism of low molecular weight proteins in the kidney during chronic mercury intoxication.
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PMID:Effects of mercury on lysosomal protein digestion in the kidney proximal tubule. 20 71

This is a study of the changes, both in serum and urine, of a wide enzymatic pattern whose origin is well known to be the renal parenchyma (LDH, LAP, AP and lysozyme), in the course of two experimental prototype lesions induced in rats. Simultaneously a similar enzymatic study was carried out in a group of patients with nephropathies. The experimental lesions were a toxic tubular dysfunction using a mercury salt and an immune glomerulonephritis of two types: by foreign proteins (human albumin) and by rabbit nephrotoxic serum. In all these cases, there has been a convincing evidence, both direct (histological and inmunofluorescent) and indirect (marked proteinuria), of the induced lesions which were similar to the experimental models reported in the literature. The isolated enzymatic changes we observed in serum made us conceed less value to this pattern in comparison to the urinary one which proved to be more important in our study. It was possible to define the following urinary enzymatic patterns for each of the experimental groups: a) The acute toxic tubular dysfunction has a marked rise in the activity of LDH and LAP, and less so in the activity of AP and lysozyme. The retarded tubular lesion has a moderate rise in LAP. b) The glomerular lesion has a moderate and exclusive rise in the activity of LDH and LAP. Likewise the clear similarity between each experimental group and its clinical equivalent was demonstrated as refers to the urinary enzymatic pattern.
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PMID:[Renal enzymology: experimental patterns and clinical symptoms]. 123 86

Glutathione (GSH)-dependent reactions are an important cellular defense against ischemic or oxidative injury, although their role in toxin-induced renal cellular injury is less clear. Because of the known sulfhydryl reactivity of mercury (M), we hypothesized that GSH could modify mercuric chloride (MC)-induced acute renal failure (ARF). Therefore, we evaluated the effects of glutathione monoethyl ester (GE), which produces high intrarenal levels of GSH, on the nephrotoxicity of MC. GE treatment in normal rats did not alter their creatinine clearance (CCr), fractional sodium (CNa/CCr) or lysozyme (CLy/CCr) excretion, but histologically resulted in prominent proximal tubular vacuolization. GE pretreatment in rats with MC-induced ARF resulted in partial preservation of their CCr, CNa/CCr and CLy/CCr. Renal histology also demonstrated a reduction in tubular necrosis. M content in the renal cortex 3 following MC was lower in the MC + GE group, but levels were higher in the liver and inner stripe/inner medulla as compared to animals receiving MC alone. No differences were seen in the outer stripe at 3 h or in any of the tissues 24 h following MC injection. Thus, GE moderated MC-induced ARF, likely by providing a large intracellular sulfhydryl pool and thereby reducing M reactivity with endogenous cellular proteins and enzymes.
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PMID:Glutathione monoethyl ester moderates mercuric chloride-induced acute renal failure. 150 44

The study was carried out in 89 men aged 21 to 57 years with a history of exposure to mercury vapour from 2 to 26 years during occupational work involving chlorine production by the method of mercury electrolysis. The workers were divided into three groups depending on the duration of occupational exposure: 1) 32 workers with a short history of exposure 2-10 years, 2) 37 workers with medium-long exposure - 11-20 years, and 3) 20 workers with a history of long exposure - 21-26 years. The urinary concentrations of mercury in these individuals was 73 +/- 60 microliters x 1(-1), and in blood this concentration was not exceeding 50 microliters x 1(-1). The control group comprised 40 men aged 17 to 52 years. They had not had any occupational exposure to chemicals, or harmful physical factors. On the basis of clinical, haematological and biochemical studies 89 workers with occupational exposure to mercury vapour were regarded as clinically healthy. None of them had any symptoms and signs of the complete neurasthenic syndrome or organic brain injury. Increased nervous excitability was the complaint of 24 workers, 9 had headaches, sleep disturbances were reported by 5, and a feeling of tiredness and apathy was mentioned by 5 men. EEG recording demonstrated 81 normal tracings, and moderately pathological records in 8 men. The parameters of immunity and proteins acute phase reaction were determined, measuring the concentration of immunoglobulins, lysozyme, C3c, C4, alpha 1-acid glycoprotein, haptoglobin and ceruloplasmin in serum. A lower level of IgA, IgG and lysozyme was only noted in individuals with occupational exposure exceeding 20 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parameters of immunity acute phase reaction in men in relation to exposure duration to mercury vapours. 172 75

The indices of immunity and acute phase reaction in 89 men exposed for 2 to 26 years to mercury vapours were assessed on the basis of immunoglobins, lysozyme, C3c, C4, alpha 1-acid glycoproteins, haptoglobin and ceruloplasmin concentrations in blood serum. Urinary mercury concentration amounted to 73 +/- 60 micrograms x l-1 whereas in blood it did not exceed 50 micrograms x l-1. A decrease in concentration of IgA, IgG and lysozyme in persons who worked for over 20 years was found. The observed phenomenon did not affect the anti-infection and antitumor immunity of the workers.
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PMID:[Indicators of immunity and acute phase reaction in men in relation to the duration of exposure to mercury vapors]. 212 72

S-mercuric-N-dansylcysteine was investigated as a potential probe of protein sulphydryl groups using bovine serum albumin, S-carboxymethyl-bovine serum albumin, lysozyme, and partially reduced lysozyme as test proteins. Criteria used to assess covalent binding through mercury-bridged mercaptide linkages include a finite reaction time (minutes to hours), abolition of the characteristic fluorescence spectrum following addition of a reducing agent, and failure to separate probe and protein after chromatography or electrophoresis. By these criteria, both Torpedo californica acetylcholinesterase and human serum cholinesterase (butyrylcholinesterase) contain four free sulphydryl groups per tetrameric enzyme molecule whereas Electrophorus electricus acetylcholinesterase has none. Labeled acetylcholinesterase and butyrylcholinesterase remain active and responsive to the inactivator Zn2+. Zn2+ promotes an increase in the fluorescence of bound S-mercuric-N-dansylcysteine, whereas activators such as Mg2+ or gallamine promote a decrease, suggesting that the label may be a useful probe of ligand-induced conformational changes. With T. californica acetylcholinesterase, but not with human serum cholinesterase, Zn2+ also promotes access to two additional groups that are reactive towards the sulphydryl reagent.
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PMID:The reaction of S-mercuric-N-dansylcysteine with acetylcholinesterase and butyrylcholinesterase. 278 87

The chemical shift changes observed in the carbon-13 NMR spectra of the carboxylate region in conjunction with previous fluorescence data indicate that mercury and lead bind to both disulfide bridge 64-80 and to Asp-52 in hen egg-white lysozyme. Methylmercury appears to bind primarily to the disulfide linkage. The carbon-13 NMR results support previous investigations by halide ion NMR and x-ray crystallography. The combined information from all of these techniques is useful for providing a clearer description of heavy metal binding to proteins.
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PMID:The detection of mercury, lead, and methylmercury binding sites on lysozyme by carbon-13 NMR chemical shifts of the carboxylate groups. 337 92

Five different cysteine-containing mutants of the lysozyme from bacteriophage T4 were used to explore the feasibility of using site-directed mutagenesis to generate isomorphous heavy-atom derivatives for protein crystallography. Cysteines 54 and 97, present in wild-type lysozyme, can be readily reacted with mercuric ion to produce an excellent isomorphous heavy-atom derivative. Mutants with an additional cysteine at position 86, 146, 153 or 157, or with Cys 97 replaced by Val, were engineered by site-directed mutagenesis. The mutant lysozyme Thr 157----Cys reacts with mercuric chloride to give an excellent new derivative although Cys 157 is only approximately 60% substituted with the heavy atom. The cysteine at position 146 is largely buried but reacts readily with mercuric chloride. In this case the isomorphism is poor and the resultant derivative is of marginal quality. Cys 153 reacts rapidly with mercuric ion but the derivative crystals do not diffract. The mutant Pro 86----Cys does not yield a particularly good heavy-atom derivative. This is due in part to a loss of isomorphism associated with the mutation. In addition, Cys 86 shows very little reactivity towards mercurials even though it is fully exposed to solvent. The mutation Cys 97----Val was used to explore the possibility of creating an independent derivative by deleting a heavy-atom site already present in wild-type lysozyme. In all cases that were tested, the quality of the heavy-atom derivative was improved by using as an isomorphous pair mercury-substituted mutant versus non-substituted mutant rather than mercury-substituted mutant versus (non-substituted) wild-type lysozyme.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of site-directed mutagenesis to obtain isomorphous heavy-atom derivatives for protein crystallography: cysteine-containing mutants of phage T4 lysozyme. 350 94

The crystal structure of baboon alpha-lactalbumin has been determined at 6 A and at 4.5 A (0.6 nm and 0.45 nm) resolution by the method of isomorphous replacement. The principal derivative was prepared by reducing a disulphide bridge in the crystals and inserting a mercury atom. Detailed comparison of the electron-density maps with corresponding maps of hen egg-white lysozyme shows that they are closely similar, with correlation coefficients of 0.57 and 0.44 at 6 A and 4.5 A resolution respectively. This result, in accordance with earlier predictions based upon comparisons of amino-acid sequences, provides further evidence that class C lysozymes and alpha-lactalbumins are homologous proteins and it is in keeping with the hypothesis that the alpha-lactalbumins evolved from a lysozyme precursor.
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PMID:Crystallographic analysis of the three-dimensional structure of baboon alpha-lactalbumin at low resolution. Homology with lysozyme. 359 55

Unilateral nephrectomy (UNX) induces a dramatic change in single-kidney structure and function. Therefore, the effects of nephrotoxins may be altered. To evaluate this possibility, mercuric chloride (2 mg/kg, sc) was given to male, Sprague-Dawley rats 2 days following either UNX or sham surgery. Nonoliguric acute renal failure developed and was qualitatively similar in both groups. Glomerular filtration rate (GFR) reached a nadir on Day 2 and was reduced to a greater extent in the UNX group. Furthermore, recovery of GFR was slower and occurred to a lesser extent by Day 10 in the animals subjected to UNX. Evidence of significant tubular dysfunction was present during the acute phase in both groups, as reflected by changes in the fractional excretion of sodium or lysozyme. Persistent tubular dysfunction was noted on Day 10 in both the sham and UNX groups, but the degree of dysfunction was greater in the UNX animals. The in vitro uptake of organic ions by renal cortical slices was reduced 24 hr following the injection of mercuric chloride although no difference was seen between the experimental groups. Mercury content within renal cortex was not increased in the UNX group at 1 or 3 hr but was higher 24 hr postinjection. Total urinary mercury excretion during the first day was not altered by UNX although single-kidney excretion was increased dramatically. These studies suggest that rats are more susceptible to mercuric chloride-induced nephrotoxicity 2 days following UNX. Although the mechanism(s) of this enhanced injury remains unclear, it does not appear to be completely related to an increase in renal cortical mercury content.
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PMID:The effect of unilateral nephrectomy on the nephrotoxicity of mercuric chloride in the rat. 370 72


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