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Biomedical subjects

J N Smith

Publications and source records attributed to J N Smith.

At least 19 recordsLinked to original sources
PubMed1995

Dating and context of three middle stone age sites with bone points in the Upper Semliki Valley, Zaire.

The extent to which the earliest anatomically modern humans in Africa exhibited behavioral and cognitive traits typical of Homo sapiens sapiens is controversial. In eastern Zaire, archaeological sites with bone points have yielded dates older than 89(-15)+22 thousand years ago by several techniques. These include electron spin resonance, thermoluminescence, optically stimulated luminescence, uranium series, and amino acid racemization. Faunal and stratigraphic data are consistent with this age.

Animals↗
PubMed1994

Selection against inbred song sparrows during a natural population bottleneck.

The genetic and demographic consequences of population subdivision have received considerable attention from conservation biologists. In particular, losses of genetic variability and reduced viability and fecundity due to inbreeding (inbreeding depression) are of concern. Studies of domestic, laboratory and zoo populations have shown inbreeding depression in a variety of traits related to fitness. Consequently, inbreeding depression is widely accepted as a fact. Recently, however, the relative impact of inbreeding on the viability of natural populations has been questioned. Work on the cheetah (Acinonyx jubatus), for example, has emphasized the overwhelming importance of environmental factors on mortality in the wild. Here we report that song sparrows (Melospiza melodia) that survived a severe population bottleneck were a non-random subset of the pre-crash population with respect to inbreeding, and that natural selection favoured outbred individuals. Thus, inbreeding depression was expressed in the face of an environmental challenge. Such challenges are also likely to be faced by inbred populations of endangered species. We suggest that environmental and genetic effects on survival may interact and, as a consequence, that their effects on individuals and populations should not be considered independently.

Animals↗
PubMed1990

Feprazone: an inducer of the P450 II B family of proteins in the rat.

The ability of feprazone to induce the hepatic microsomal mixed-function oxidases was investigated in the rat, with emphasis being placed on the nature of the cytochrome P-450 family induced. Treatment with feprazone enhanced the p-hydroxylation of aniline and the dealkylations of benzphetamine and pentoxyresorufin but had no effect on the O-deethylation of ethoxyresorufin. The same treatment had no major effect on total cytochrome P-450 levels but increased the spectral interaction of metyrapone with reduced cytochrome P-450. Immunoblots employing monospecific polyclonal antibodies revealed that feprazone induces the apoprotein levels of the P450 II B, but not of the P450 I, family. It is concluded that feprazone is an inducer of the rat hepatic mixed-function oxidase system showing selectivity toward the P450 II B family.

Animals↗
PubMed1988

Induction of the rat hepatic microsomal mixed-function oxidases by two aza-arenes. A comparison with their non-heterocyclic analogues.

The ability of the aza-aromatic polycyclic aromatic hydrocarbons 10-azobenz(a)pyrene and benz(a)acridine to induce the rat hepatic microsomal mixed-function oxidases was compared to that of their non-heterocyclic analogues benz(a)pyrene and benz(a)anthracene respectively. All four hydrocarbons markedly increased the O-deethylations of ethoxyresorufin and ethoxycoumarin, the non-heterocyclic analogues being the more potent. A more modest increase was seen in the O-dealkylation of pentoxyresorufin. All four hydrocarbons induced proteins recognised by antibodies to cytochrome P-450IAI but no increase was seen when antibodies to cytochrome P-450IIB1 were employed. The metabolic activation of benz(a)pyrene and Glu-P-1 to mutagenic intermediates in the Ames test was enhanced by all pretreatments. It is concluded that the aza-aromatic polycyclic hydrocarbons, like their non-heterocyclic analogues, selectively induce the cytochrome P-450I family of proteins.

Acridines↗
PubMed1987

Bioactivation of N-nitrosopiperidine to mutagens: role of hepatic cytochrome P-450 proteins and contribution of cytosolic fraction.

In the present study the role of two families of cytochrome P-450 proteins and the contribution of the cytosolic fraction in the activation of N-nitrosopiperidine to mutagens in the Ames test were investigated. The bioactivation of this nitrosamine was preferentially catalysed by the phenobarbitone-induced cytochromes P-450, in contrast to the 3-methylcholanthrene-induced cytochromes P-448. The mutagenicity of nitrosopiperidine catalysed by microsomes, in the absence of cytosol, was lower when compared with that observed with S9 fractions. Cytosol itself could not activate nitrosopiperidine but potentiated the microsome-mediated mutagenicity of the carcinogen. The cytosolic potentiation was still evident when microsomal metabolism was terminated, indicating that cytosolic enzyme(s) can further convert the microsome-generated metabolites to more potent mutagens. The cytosolic enzyme(s) was inducible by prior treatment of the rats with phenobarbitone or Arochlor 1254 but not 3-methylcholanthrene. The microsome-mediated activation of nitrosopiperidine could be supported by NADH in the absence of NADPH. It is therefore concluded that the activation of nitrosopiperidine to mutagen(s) involves, in addition to NADH- and NADPH-dependent microsomal enzymes, cytosolic proteins.

Animals↗
PubMed1987

Cytosolic potentiation of the rat hepatic microsome mediated mutagenicity of benzidine.

The role of the cytosolic fraction in the S9-mediated metabolic activation of benzidine to mutagens in the Ames test was investigated using hamster and rat hepatic preparations. Rat microsomes alone were poor activators of benzidine compared to hamster microsomes, at least partly explaining the well known superiority of S9 preparations from the latter species in activating this amine. Supplementation of rat microsomal preparations with the cytosolic fraction from hamsters and to a lesser extent from rats enhanced the bioactivation of benzidine. When hamster microsomal preparations were supplemented with rat or hamster cytosolic fractions no significant effect was observed. Cytosolic fractions from either species could not activate benzidine to mutagens in the absence of microsomes. The cytosolic potentiation of the microsome-mediated activation of the amine was not inducible by Aroclor 1254. Similarly, the microsome-mediated activation of benzidine was not enhanced by Aroclor 1254 pre-treatment of the rats, when mutagenicity is expressed per nmol of cytochrome P-450. It is concluded that (i) the cytosolic fraction may play an important role in the metabolic activation by S9 preparations of chemical carcinogens such as benzidine, and (ii) the Aroclor-induced isozymes of cytochrome P-450 do not catalyse the N-hydroxylation of benzidine.

Animals↗
PubMed1987

Induction of the hepatic mixed-function oxidases by Aroclor 1254 in the hamster: comparison of Aroclor-induced rat and hamster preparations in the activation of pre-carcinogens in the Ames test.

Hepatic microsomal mixed-function oxidase activities and the metabolic activation of chemical carcinogens to mutagens in the Ames test were investigated using Aroclor 1254-induced rat and hamster preparations. Benzphetamine N-demethylase, NADPH-cytochrome c reductase and cytochromes P-450 and b5 were induced in both animals to the same extent by pre-treatment with Aroclor. However, the O-deethylation of ethoxyresorufin was markedly induced in the rat (147-fold) but only modestly in the hamster (3-fold). 1,2-Benzanthracene and 4-aminobiphenyl were more efficiently activated by the rat preparations while, in contrast, 2-acetylaminofluorene, 2-aminoanthracene, nitrosopiperidine, nitrosopyrrolidine, cyclophosphamide and phenacetin were more efficiently activated by the hamster preparations. No significant difference was observed in the activation of 3-methylcholanthrene, benzo[a]pyrene and 2-aminofluorene. It is concluded that (a) the hamster is relatively refractive to cytochrome P-448 induction, and (b) Aroclor 1254-induced rat and hamster S9 preparations differ in their ability to convert chemical carcinogens to mutagens in the Ames test.

Animals↗
PubMed1987

Seasonal changes in density and tissue distribution of Onchocerca cervicalis microfilariae in ponies and related changes in Culicoides variipennis populations in Louisiana.

Seasonal changes in density and spatial distribution of Onchocerca cervicalis microfilariae were studied in ventral-midline skin of 15 infected pony mares in southern Louisiana. Triple running mean analysis of data over a 13-mo period indicated that a distinct pattern exists in total microfilariae population density and in microfilariae occurrence in different levels of the dermis. Microfilariae density reaches peak levels in the spring followed by a 58% decrease in the summer, a 19% increase in the fall, and a decrease to the lowest numbers in the winter. Microfilariae were found in all levels of the skin during the spring, summer, and fall but were not found in the superficial layers of the dermis during the winter months. The population density of Culicoides variipennis, a demonstrated vector of O. cervicalis, appeared to have seasonal fluctuations similar to the changes in microfilarial density. Harmonic wave analysis of microfilariae density data in individual ponies showed that all individuals did not follow the population trend.

Animals↗
PubMed1984

Kinetic studies on a glutathione S-transferase from the larvae of Costelytra zealandica.

Of the glutathione S-transferases from the New Zealand grass grub (Costelytra zealandica) active in conjugating the model substrate 1-chloro-2,4-dinitrobenzene, the most active was isolated in a functionally homogeneous form. This had an isoelectric point of 8.7. Preliminary evidence suggests that it is a homodimer with subunits of Mr 23 500. The dependence of the enzyme-catalysed reaction on substrate concentration was analysed in terms of the rate equation characteristic of Ordered Bi Bi or Rapid-Equilibrium Random mechanisms. Evidence was found for a critical ionizing event at pH 9.3 at 37 degrees C. This event appears to involve a twofold change in charge on the enzyme, which may be the result of co-operative ionizations rather than independent ionizations. This appears to affect neither the binding of the aromatic substrate to the enzyme, nor the maximum catalytic velocity of the enzyme-catalysed reaction. The variation of the kinetics with temperature was studied. Apparent thermodynamic parameters characteristic of the reaction were derived. The possible relevance of the temperature-dependence of the enzyme-catalysed reaction in vivo is discussed.

Animals↗
PubMed1983

Acidic conjugate of phenols in insects; glucoside phosphate and glucoside sulphate derivatives.

Conjugates of p-nitrophenol in nine species of insects were identified by paper chromatography and ionophoresis as the glucoside, the sulphate, the phosphate and the glucoside phosphate. Metabolites with similar properties to the glucoside phosphates were also formed from 8-hydroxyquinoline, 1-naphthol and 4-methylumbelliferone in Tenebrio larvae. Tenebrio larvae also metabolized p-nitrophenol to a compound believed to be p-nitrophenyl glucoside-6-sulphate. None of the nine species of insect used was able to metabolize [14C]benzoic acid to a glucoside-phosphate or glucoside-sulphate conjugate.

Animals↗
PubMed1981

Inhibition of housefly oxidative detoxication by phthaleins, fluoresceins and related compounds.

1. Phenolphthalein, halogenated fluoresceins, and other triphenylmethane and diphenylmethane derivatives inhibited biphenyl hydroxylation, aldrin epoxidation and several O-dealkylations in insect abdomen homogenates. Phenolphthalein and eosin (50 muM) were 2-3 times more effective than SKF 525-A and piperonyl butoxide (50 muM) as inhibitors of biphenyl hydroxylation in vitro. 2. The phthaleins, Aurin and Aluminon, inhibited both epoxidation and hydroxylation to similar extents, but fluoresceins, Rhodamine B, Malachite Green, and basic diphenylmethane derivatives preferentially inhibited hydroxylation. 3. Tetrabromophenolphthalein ethyl ester and bis-(N-dimethyl-4-aminophenyl-methane inhibited biphenyl hydroxylation in vivo. Bis-(N-dimethyl-4-aminophenyl) methane synergized the toxic effects of 1-naphthyl N-methylcarbamate in live houseflies.

Abdomen↗