Effect of environmental factors on drug metabolism: Decreased plasma half‐life of antipyrine in workers exposed to chlorinated hydrocarbon insecticides

Kolmodin, Birgitta; Azarnoff, Daniel L.; Sjöqvist, Folke

doi:10.1002/cpt1969105638

Cited by 185 publications

(46 citation statements)

References 10 publications

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“…Drugs that inhibit oxidation include isoniazid (Kutt, Winters & McDowell, 1966), some sulphonamides (Christensen, Hansen & Kristensen, 1962), and chloramphenicol (Christensen & Skovsted, 1969). Environmental factors that increase the rate of drug oxidation include occupational exposure to chlorinated hydrocarbon insecticides (Kolmodin, Azarnoff & Sjoqvist, 1969), anaesthetic gases (O'Malley, Stevenson & Wood, 1973) and cigarette smoke (Hart, Farrell, Cooksley & Powell, 1976;Vestal, Norris, Tobin, Cohen, Shock & Adres, 1975). The steroidal oral contraceptive pill inhibits drug oxidation (O'Malley, Stevenson & Crooks, 1973).…”

Section: Introductionmentioning

confidence: 99%

Environmental factors affecting antipyrine metabolism in London factory and office workers.

Fraser¹,

Mucklow²,

Bulpitt³

et al. 1979

Brit J Clinical Pharma

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Section: Introductionmentioning

confidence: 99%

Environmental factors affecting antipyrine metabolism in London factory and office workers.

Fraser¹,

Mucklow²,

Bulpitt³

et al. 1979

Brit J Clinical Pharma

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“…Antipyrine is extensively oxidized by the liver (Brodie & Axelrod, 1950;Yoshimura, Shimeno & Tsukamoto, 1968) and is only 10% bound to plasma proteins (Soberman, Brodie, Levy, Axelrod, Hollander & Steele, 1949); it is distributed throughout body water and less than 5% of the dose is excreted in the urine in 24 h (Brodie & Axelrod, 1950). For these reasons, the plasma half-life of antipyrine is widely used as an index of drug oxidation (Vessel & Page, 1969;Kolmodin, Azarnoff & Sjoqvist, 1969;Breckenridge, Orme, Thorgeirsson, Davies & Brooks, 1971;O'Malley, Stevenson & Crooks, 1972 (Nos. 5,8,9,10,11 and 12) for several months.…”

Section: Introductionmentioning

confidence: 99%

The plasma half‐life of antipyrine in chromic uraemic and normal subjects.

Maddocks¹,

Wake²,

Mj³

1975

Brit J Clinical Pharma

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1. Antipyrine was given intravenously in a dose of 18 mg/kg body weight to twelve patients with chronic renal failure (plasma creatinine greater than 4.9 mg/100 ml) who were not taking drugs and twenty normal subjects. 2. Plasma antipyrine levels were measured by a specific method, the plasma half‐life of the drug was determined and used as an index of drug oxidation. 3. The mean (+/‐ s.d) plasma antipyrine half‐ life in patients with chronic renal failure (7.3 +/‐ 2.0 h) was significantly shorter than in normal subjects (13.2 +/‐ 4.3 h: P less than 0.002). There was no difference in the apparent volume of distribution of antipyrine between the two groups (P greater than 0.6). 4. Pretreatment of five patients with chronic renal failure and seven normal subjects with antipyrine or phenobarbitone for weeks significantly shortened the mean plasma antipyrine half‐life from 7.4 +/‐ 2.5 h to 5.0 +/‐ 1.5 h in uraemics (P less than 0.005) and from 13.2 +/‐ 4.5 h to 6.9 +/‐ 1.5 h in normal subjects (P less than 0.0025).5. These results suggest that oxidation of antipyrine by hepatic microsomal enzymes is increased in patients with chronic renal failure, but a state of maximal induction of these enzymes was not observed. The clinical implication of this finding with regard to the association between liver microsomal enzyme induction and vitamin D resistant osteomalacia is discussed.

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“…However, polyaromatic hydrocarbons such as polychlorinated biphenyls and various pesticides are well established inducers of antipyrine (1,13) and phenylbutazone metabolism (19). Also the anesthetic agent halothane may be an inducer of antipyrine metabolism (5,6).…”

Section: Discussionmentioning

confidence: 99%

Jet fuel and liver function.

Døssing¹,

Loft²,

Schroeder³

1985

Scand J Work Environ Health

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, MD2D0SSING M, LOFT S, SCHROEDER E. Jet fuel and liver function. Scand J Work Environ Health II (1985) 433-437. The impact of occupational exposure to jet fuel on antipyrineelimination wasstudied in 91 fuel-filling attendants. The mean antipyrine clearancewas enhancedto 68.4 (SD 19.5)ml/min during exposure to jet fuel compared to 57.9 (SD 18.1)ml/min after an exposure-free period of two to four weeks. The correspondingvalues for 47 office workers (referents) were 62.7 (SD 22.2) ml/min and 56.4 (SD 22.3) ml/min. The median jet fuel concentration in the breathing zone of the fuel-filling attendants was 31 (range I-I 020) mg/rn-. No known inducing factor could be identified in the work environment ofthe office workers. No difference in the concentration of aspartate aminotransferase and alkaline phosphatase in serum was found either within or between the groups. Our study indicates that jet fuel, which is a mixture of aliphatic and aromatic organic solvents resembling gasoline and white spirit, is an inducer of hepatic drug metabolism in man.

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Effect of environmental factors on drug metabolism: Decreased plasma half‐life of antipyrine in workers exposed to chlorinated hydrocarbon insecticides

Cited by 185 publications

References 10 publications

Environmental factors affecting antipyrine metabolism in London factory and office workers.

Environmental factors affecting antipyrine metabolism in London factory and office workers.

The plasma half‐life of antipyrine in chromic uraemic and normal subjects.

Jet fuel and liver function.

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