Effects of triethyl lead administration on the expression of glutathione S-transferase isoenzymes and quinone reductase in rat kidney and liver

Daggett, Daniel A.; Nuwaysir, Emile F.; Nelson, Shelli A.; Wright, Lynda S.; Kornguth, Steven; Siegel, Frank L.

doi:10.1016/s0300-483x(96)03555-x

Cited by 20 publications

(13 citation statements)

References 33 publications

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“…The inhibited activity of the GST in the liver in Pbtreated rats is in accordance with the previous observations that Pb-intoxicated rats exhibit a decrease in hepatic GST activity [37]. This enzyme catalyzes the conjugation of GSH with a large variety of toxic and carcinogenic compounds [38].…”

Section: Effect Of Leadsupporting

confidence: 91%

Prophylactic effect of melatonin on lead-induced inhibition of heme biosynthesis and deterioration of antioxidant systems in male rats

El-Missiry

2000

J. Biochem. Toxicol.

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We studied the protective role of the pineal hormone melatonin on lead‐induced suppression of the heme synthesis pathway as a consequence of reduced antioxidant systems in rat. We injected rats intramuscularly with lead acetate (10 mg/kg body weight) daily for 7 days, which significantly abolished heme synthesis as evidenced by decreased blood hemoglobin, liver δ‐aminolevulinic acid synthetase, erythrocytic δ‐aminolevulinic acid dehydratase, and hepatic iron content. These effects were accompanied with marked elevation of hepatic lipid peroxidation and decreased enzymatic antioxidants such as glutathione reductase, glutathione‐S‐transferase, superoxide dismutase, and catalase, as well as nonenzymatic antioxidants such as total sulfhydryl groups and glutathione. Furthermore, lead treatment caused hepatic deficiency in copper and zinc accompanied by a significant elevation of lead concentration in both plasma and liver. Daily pretreatment with melatonin (30 mg/kg body weight) intragastrically prevented the suppressive effects of lead on heme‐synthesizing enzymes and iron deficiency. In addition, preadministration of melatonin reduced the inhibitory effect of lead on both enzymatic and nonenzymatic antioxidants. This was accompanied by marked normalization of lipid peroxidation and modulation of copper and zinc levels in liver. The action of melatonin on lead‐induced changes was attributed to protection of the antioxidant capacity in cells in addition to the ability of melatonin to scavenge free radicals. © 1999 John Wiley & Sons, Inc. J Biochem Toxicol 14: 57–62, 2000

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Section: Effect Of Leadsupporting

confidence: 91%

Prophylactic effect of melatonin on lead-induced inhibition of heme biosynthesis and deterioration of antioxidant systems in male rats

El-Missiry

2000

J. Biochem. Toxicol.

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“…Animals were dosed on a mg/kg basis as follows: 260, 360, or 1300 ug/kg lead to achieve targeted blood levels of 20, 40 or 80 ug/dL. Following the loading dose period, rabbits were then placed on a maintenance dose solutions during study weeks [11][12][13][14][15][16][17][18][19][20] Dayton OH. Warm and cold ischemic times were 10 and 50 min, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…GSTs are a family of detoxification isoenzymes that catalyze the conjugation of xenobiotics and their metabolites with reduced glutathione and thus constitute an important defense mechanism against chemical toxicity. Lead exposure in rats is known to induce 7t-class GST (GSTP1) in the liver and almost all GST isoforms in the kidney [20]. The cytosolic family of GSTs consists of several families (a, u, JI, a and 0) with catalytically active…”

Section: Introductionmentioning

confidence: 99%

Protein Markers of Chemical Exposure and Molecular Epidemiology

Witzmann¹

1999

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PubKc reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources gathering and rnaintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect Of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 222024302, and to the Office of Management and Budget, Paperwork Reduction Project (0704-0188), Washington, DC 20503. AGENCY USE ONLY (Leave Blank)2. REPORT DATE July 30,1999 TITLE AND SUBTITLE Protein Markers of Chemical Exposure and Molecular Epidemiology AUTHOR(S)Frank A. Witzmann PERFORMING ORGANIZATION NAME(S) AND ADDRESSES)Molecular Anatomy Laboratory, Dept of Biology Indiana University Purdue University -Columbus 4601 Central Avenue Columbus IN 47203 SPONSORINGyMONITORING AGENCY NAME(S) AND ADDRESS(ES)AFOSR 12b. DISTRIBUTION CODE ABSTRACT (Maximum 200 words)This final technical report describes the results of experiments that 1) explored, at the molecular level, the toxicity of lead in various exposure systems; 2) enabled the development a system of general and tissue-specific protein markers for lead in rabbits and rats that might be indicative of its effect in human toxicologic targets; 3) assessed the cellular expression of GST isoenzymes as protein markers of lead toxicity in rat kidney, and 4) investigated the suitability of tissue-slice in vitro toxicologic approaches by evaluating their patterns of protein expression and comparing them to patterns from whole tissues. High resolution large-scale two-dimensional polyacrylamide gel electrophoresis (2-DE) with computerized image analysis was used to map cell/tissue proteins of various lead targets. In the case of lead experiments, proteomics technology, e.g. mass spectrometric analysis of tryptic digests (peptide-mass fingerprinting) of selected proteins resolved by 2-DE , was used to identify altered proteins. Quantitative and qualitative assessments of toxic effect were made, individual protein data was compiled in annotated databases, and protein markers identified. Protein digestion 9 Matrix-assisted laser desorption mass spectrometric (MALDI) protein identification 9 SUBJECT TERMSResults and Discussion 1" Toxicity of lead in rabbit ventricle and kidney 10 Assessment of regional differences in renal lead toxicity 12 Assessment of glutathione S-transferase (GST) isoenzyme expression 14 AbstractThis final technical report describes the results of experiments that 1) explored, at the molecular level, the toxicity of lead in various exposure systems; 2) enabled the development a system of general and tissuespecific protein markers for lead in rabbits and rats that might be indicative of its effect in human toxicologic targets; 3) assessed the cellular expression of GST isoenzymes as ...

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“…slight deficits in attention span and learning abilities. In adults, lead can increase blood pressure and cause fertility problems, nerve disorders, muscle and joint pain, irritability, and memory or concentration problems [3][4][5][6][7][8]. Thus, the concentration of lead in environment should be kept under permanent control.…”

Section: Introductionmentioning

confidence: 99%