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Biomedical subjects

J G Wit

Publications and source records attributed to J G Wit.

13 recordsLinked to original sources
PubMed1976

Ferrihemoglobin formation by monohydroxy aniline derivatives in erythrocytes of some avian species in comparison with mammals.

Ferrihemoglobin formation nitrosobenzene and p-, m- and o-animophenol was studied in erythrocyte supspensions from a number of avian and mammalian species. Compared with the mammalian erythrocytes, bird red cells show little species differences in susceptibility. In birds, dose-effect relationship are different for nitrosobenzene and the aminophenols: using low concentration nitrosobenzene is more active than the aminophenols, while at higher concentrations o-aminophenol is at least equally effective. In birds, o-aminophenol is about eight times more potent than p-aminophenol. m-Anminophenol is not an inducer of ferrihemoglobin in erythrocytes of the cat, the goat and the Japanese quail.

Aniline Compounds↗
PubMed1975

Nitrosobenzene-induced ferrihemoglobin formation in Japanese quail erythrocytes. The significance of ferrihemoglobin reduction.

Quantitative aspects of nitrosobenzene-induced ferrihemoglobin formation were studied in quail erythrocytes in comparison to goat red cells. Many similarities exist with the mechanism in mammalian red cells such as a NADPH-dependent enzymatic recycling of phenylhydroxylamine from nitrosobenzene. Also the mechanism of ferrihemoglobin reduction is similar in both species, it is a NADH-dependent process. However, the reducing activity of quail red cells exceeds by far the activity of the majority of mammalian erythrocytes.

Animals↗
PubMed1966

Metabolism of the herbicide 2,6-dichlorobenzonitrile in rabbits and rats.

1. The metabolism of 2,6-dichlorobenzonitrile was studied in rabbits and rats. Oral administration caused an increased urinary excretion of glucuronides and ethereal sulphates. There was also an indication of mercapturic acid formation. 2,6-Dichloro-3-hydroxybenzonitrile and its 4-hydroxy analogue were identified as metabolites in the urine. A small amount of the unchanged substance was recovered from the faeces. 2. By using 2,6-dichlorobenzo[(14)C]nitrile the phenolic metabolites were determined quantitatively and some other possible metabolic routes were excluded. 3. Incubation of 2,6-dichlorobenzonitrile with enzyme preparations (papain and high-speed supernatant of rat-liver homogenate plus glutathione) gave no indications for a reaction with thiol compounds.

Journal Article↗
PubMed1966

The monophenolic metabolites of the herbicide 2,6-dichlorobenzonitrile in animals as uncouplers of oxidative phosphorylation.

1. Both monophenolic metabolites of 2,6-dichlorobenzonitrile (2,6-dichloro-3-hydroxybenzonitrile and its 4-hydroxy analogue) added to starved yeast cells incubated with a limited quantity of glucose cause a significant rise in oxygen consumption of the cells. 2. The same compounds induce adenosine-triphosphatase activity in isolated intact rat-liver mitochondria. 3. The possible role of the hydroxylation of 2,6-dichlorobenzonitrile in mammals in relation to hepatic injury is discussed.

Journal Article↗
PubMedDate not supplied

Effects of phenylhydroxylamine and aminophenols in Japanese quail in vivo.

1. The effects of phenylhydroxylamine, and o- and p-aminophenol were studied in the Japanese quail. 2. Symptoms normally observed in aniline-treated birds were seen in quail after phenylhydroxylamine dosage at > 10 mg/kg. Aminophenols (up to 50 mg/kg) did not give these symptoms. 3. Injection of phenylhydroxylamine (50 mg/kg) resulted in formation of 70% ferrihaemoglobin after 5 min, following which a rapid reduction of ferrihaemoglobin was observed. 4. Phenylhydroxylamine reached highest blood concn. of 0.2 mumol/ml after 5 min. Phenylhydroxylamine was reduced to aniline within 5 min. 5. The effects of aniline in vivo are most probably due to O2 shortage caused by ferrihaemoglobin formation.

Aminophenols↗