Spectrophotometric assays for the enzymatic hydrolysis of the active metabolites of chlorpyrifos and parathion by plasma paraoxonase/arylesterase

Furlong, Clement E.; Richter, Rebecca J.; Seidel, Sharon L.; Costa, Lucio G.; Motulsky, Arno G.

doi:10.1016/0003-2697(89)90424-7

Cited by 210 publications

(145 citation statements)

References 5 publications

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“…Erythrocyte glutathione was measured with an assay kit (Calbiochem, San Diego, CA). Serum paraoxonase activity was determined spectrophotometrically at 270 nm with phenylacetate as the substrate (18).…”

Section: Methodsmentioning

confidence: 99%

α-Lipoic Acid Prevents the Increase in Atherosclerosis Induced by Diabetes in Apolipoprotein E–Deficient Mice Fed High-Fat/Low-Cholesterol Diet

Maeda

2006

Diabetes

105

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Considerable evidence indicates that hyperglycemia increases oxidative stress and contributes to the increased incidence of atherosclerosis and cardiovascular complications in diabetic patients. To examine the effect of ␣-lipoic acid, a potent natural antioxidant, on atherosclerosis in diabetic mice, 3-month-old apolipoprotein (apo) E-deficient (apoE ؊/؊ ) mice were made diabetic by administering streptozotocin (STZ). At 4 weeks after starting the STZ administration, a high-fat diet with or without ␣-lipoic acid (1.65 g/kg) was given to the mice and to nondiabetic apoE ؊/؊ controls. At 20 weeks, markers of oxidative stress were significantly lower in both the diabetic apoE ؊/؊ mice and their nondiabetic apoE ؊/؊ controls with ␣-lipoic acid supplement than in those without it. Remarkably, ␣-lipoic acid completely prevented the increase in plasma total cholesterol, atherosclerotic lesions, and the general deterioration of health caused by diabetes. These protective effects of ␣-lipoic acid were accompanied by a reduction of plasma glucose and an accelerated recovery of insulinproducing cells in the pancreas, suggesting that part of its effects are attributable to protecting pancreatic ␤-cells from damage. Our results suggest that dietary ␣-lipoic acid is a promising protective agent for reducing cardiovascular complications of diabetes. Diabetes

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Section: Methodsmentioning

confidence: 99%

α-Lipoic Acid Prevents the Increase in Atherosclerosis Induced by Diabetes in Apolipoprotein E–Deficient Mice Fed High-Fat/Low-Cholesterol Diet

Maeda

2006

Diabetes

105

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“…There was a mean 4.4% variation between assays for these 29 samples. The assay results for the three substrates permitted separation of activity levels, providing determination of the inferred genotype of each subject's PON1 (Furlong et al, 1989;Davies et al, 1996;Richter and Furlong, 1999). PON1 inferred genotypes were determined from two-dimensional enzyme plots showing the rates of hydrolysis of chlorpyrifos oxon and of diazoxon plotted against the rates of hydrolysis of paraoxon for each subject's plasma.…”

Section: Pon1 Inferred Genotype and Chlorpyrifosoxonase Activitymentioning

confidence: 99%

Paraoxonase status and plasma butyrylcholinesterase activity in chlorpyrifos manufacturing workers

Albers

Garabrant

Berent

et al. 2009

J Expo Sci Environ Epidemiol

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Chlorpyrifos is an organophosphorus (OP) anticholinesterase insecticide. Paraoxonase (PON1) is an enzyme found in liver and plasma that hydrolyzes a number of OP compounds. PON1 polymorphisms include a glutamine (Q)/arginine (R) substitution at position 192 (PON1 Q192R ) that affects hydrolysis of OP substrates, with the PON1 192Q allotype hydrolyzing chlorpyrifos oxon less efficiently than the PON1 192R allotype, a variation potentially important in determining susceptibility to chlorpyrifos. We studied 53 chlorpyrifos workers and 60 referents during 1 year and estimated chlorpyrifos exposure using industrial hygiene and employment records and excretion of the chlorpyrifos metabolite 3,5,6-trichloro-2-pyridinol (TCP). Plasma butyrylcholinesterase (BuChE) activity, which may by inhibited by chlorpyrifos exposure, was measured monthly. In addition, plasma samples were assayed for paraoxonase (PONase), diazoxonase (DZOase), and chlorpyrifosoxonase (CPOase) activity to determine PON1 status (inferred genotypes and their functional activity). Linear regression analyses modeled BuChE activity as a function of chlorpyrifos exposure and covariates. We postulated that the level of CPOase activity and the inferred PON1 192 genotype (together reflecting PON1 status) would differ between groups and that PON1 status would modify the models of chlorpyrifos exposure on BuChE activity. Chlorpyrifos workers and referents had a 100-fold difference in cumulative chlorpyrifos exposure. Contrary to our hypotheses, mean CPOase activity was similar in both groups (P ¼ 0.58) and PON1 192Q showed a slight overrepresentation, not an underrepresentation, in the chlorpyrifos group compared with referents (PON1 192QQ , 51% chlorpyrifos, 40% referent; PON 192QR , 43% chlorpyrifos, 40% referent; PON 192RR , 6% chlorpyrifos, 20% referent, P ¼ 0.08). In our models, BuChE activity was significantly inversely associated with measures of interim chlorpyrifos exposure, but the biological effects of chlorpyrifos exposure on BuChE activity were not modified by PON1 inferred genotype or CPOase activity.

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“…Paraoxonase (PON) activity in the plasma and lipoprotein fractions was determined by an adaptation of the spectrophotometric method of Furlong et al 38 …”

Section: Determination Of Pon Activitymentioning

confidence: 99%

Hyperbaric Oxygen Reduces the Progression and Accelerates the Regression of Atherosclerosis in Rabbits

Kudchodkar

Wilson

Lacko

et al. 2000

ATVB

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Abstract-We studied the effect of hyperbaric oxygen (HBO) treatment on the extent of diet-induced accumulation of lipid oxidation products in rabbit plasma and tissues, on plasma paraoxonase activity, and on the extent of progression and regression of atherosclerotic lesions in the rabbit aorta. HBO treatment of cholesterol-fed rabbits dramatically reduces the development of arterial lesions despite having little or no effect on plasma or individual lipoprotein cholesterol concentrations. Compared with no treatment in cholesterol-fed animals, HBO treatment also substantially reduces the accumulation of lipid oxidation products (conjugated dienes, trienes, and thiobarbituric acid-reactive substances) in plasma, in the low density lipoprotein and high density lipoprotein fractions of plasma, in the liver, and in the aortic tissues. In addition, HBO treatment prevents the decrease in plasma paraoxonase activity observed in rabbits fed cholesterol-rich diets. Similarly, in regression studies, HBO treatment has no effect on the rate of plasma (or lipoprotein) cholesterol decline but significantly accelerates aortic lesion regression compared with no treatment. Direct measures of aortic cholesterol content support these morphological observations. On the basis of these results, we conclude that repeated, but relatively short, exposure to HBO induces an antioxidant defense mechanism(s) that is responsible for retarding the development or accelerating the regression of atherosclerotic lesions.

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Spectrophotometric assays for the enzymatic hydrolysis of the active metabolites of chlorpyrifos and parathion by plasma paraoxonase/arylesterase

Cited by 210 publications

References 5 publications

α-Lipoic Acid Prevents the Increase in Atherosclerosis Induced by Diabetes in Apolipoprotein E–Deficient Mice Fed High-Fat/Low-Cholesterol Diet

α-Lipoic Acid Prevents the Increase in Atherosclerosis Induced by Diabetes in Apolipoprotein E–Deficient Mice Fed High-Fat/Low-Cholesterol Diet

Paraoxonase status and plasma butyrylcholinesterase activity in chlorpyrifos manufacturing workers

Hyperbaric Oxygen Reduces the Progression and Accelerates the Regression of Atherosclerosis in Rabbits

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