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Biomedical subjects

P J Gehring

Publications and source records attributed to P J Gehring.

At least 37 records · Page 2Linked to original sources
PubMed1977

The fate of 2,4-dichlorophenoxyacetic acid (2,4-D) following oral administration to man.

The pharmacokinetic profile of 2,4-D is defined in man. Five male human volunteers ingested a single dose of 5 mg/kg 2,4-D without detectable clinical effects. Concentration of 2,4-D were determined in plasma in 3 of 5 subjects and in urine in all subjects at intervals after ingestion. The elimination of 2,4-D from plasma in all subjects occurred by an apparent first-order rate process with an average half-life (t1/2) of 11.6 h. All subjects excreted 2,4-D in the urine with an average t1/2 of 17.7 h. Excretion occurred mainly as 2,4-D (82.3%) with smaller amounts excreted as a 2,4-D conjugate (12.8%). Essentially all of the 2,4-D was absorbed from the gastrointestinal tract in man. Clearance of 2,4-D from the plasma and excretion from the body are first-order rate processes. There was no evidence that 2,4-D would accumulate following repeated administration.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1977

Fate of silvex following oral administration to humans.

The fate of silvex [2-(2,4,5-trichlorophenoxy)propionic acid] was defined in seven men and in one woman following oral administration of 1 mg/kg. No adverse effects were observed. Samples of blood plasma, urine, and feces were collected at designated time intervals through 168 hr. Plasma samples were analyzed for silvex only, while samples of urine and feces were analyzed for silvex, silvex conjugate(s), 2,4,5-trichlorophenol, and 2,4,5-trichlorophenol conjugate(s). Apparent first-order kinetics described the biphasic clearance of silvex from plasma and excretion in urine. The half-life values for clearance of silvex from plasma were 4.0 +/- 1.9 and 16.5 +/- 7.3 hr for the initial and terminal phases, respectively. Peak plasma levels of silvex occurred within 2-4 hr after dosage. Within 24 hr after administration, 65% of the administered dose had been excreted in urine. Silvex was excreted in urine as silvex and silvex conjugate(s). The half-life values for excretion of silvex per se in urine were 5.0 +/- 1.8 and 25.9 +/- 6.3 hr for the two phases, respectively. Small amounts (3.2% or less) of silvex and/or silvex conjugate(s) were eliminated in feces. Recovery of silvex and its conjugate(s) in urine and feces through 168 hr ranged from 66.6 to 95.1% of the administered dose, with a mean value and standard deviation of 80.3 +/- 10.5%. In humans, silvex is readily absorbed after ingestion and subsequently readily excreted, predominantly via the urine.

Administration, Oral↗
PubMed1977

Pharmacokinetics of vinylidene chloride in the rat.

The metabolism of inhaled vinylidene chloride in rats represents a balance of biotransformation pathways leading to the formation of a reactive alkylating species which is normally detoxified by conjugation with glutathione. Detoxification of the reactive intermediate formed from inhaled VDC is dependent upon the availability of hepatic glutathione (GSH); as VDC exposure concentrations are increased, the fraction of the dose detoxified by conjugation with GSH decreases markedly, commensurate with depletion of hepatic GSH. This reactive intermediate in the absence of GSH alkylates hepatic macromolecules and causes cell death. Similarly, hepatic GSH plays a vital role in the detoxification of the reactive metabolite formed from inhaled vinyl chloride (VC). However, the dose--response relationships for the utilization of GSH and the accumulation of alkylating metabolites following inhalation exposure to either VDC or VC point to distinct differences which may explain the differing biological activities of the two materials. Finally, preliminary pharmacokinetic data for inhaled VDC in mice indicate an enhanced susceptibility to VDC by virtue of an increased ability for production of alkylating VDC metabolites over that observed in the rat. The importance of these findings in light of recent evidence for a carcinogenic effect of VDC in mice is discussed.

Animals↗
PubMed1976

Vinyl chloride-induced depression of hepatic non-protein sulfhydryl content and effects on bromosulphalein (BSP) clearance in rats.

Rats were exposed to atmospheres of 2000, 1000, 250, 150, 50 and 10 ppm vinyl chloride (VC) for 1-7 h to determine the effect of VC on the hepatic non-protein sulhydryl content, Exposure to 2000, 1000, 250 and 150 ppm VC caused a progressive depression of the hepatic non-protein sulfhydryl content. Following exposure to 50 ppm VC for 7 h the depression was inconsistent, and no depression was observed after 10 ppm VC for 7 h. Also, exposure to 1000 ppm VC did not alter the serum clearance of bromosulphalein (BSP).

Animals↗