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D W Nebert

Publications and source records attributed to D W Nebert.

At least 325 records · Page 18Linked to original sources

Stimulation of aryl hydrocarbon hydroxylase induction in cell cultures by interferon.

In cell cultures previously treated with homologous interferon, the magnitude of antiviral activity and the degree of stimulation of aryl hydrocarbon hydroxylase induction appear to be directly related. In a highly purified mouse interferon preparation, the factor stimulating hydroxylase induction and the factor directing antiviral activity are inactivated by heating to 70 C or by treating with trypsin. Also, both activities demonstrate species specificity.

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Expression of aryl hydrocarbon hydroxylase induction and suppression of tyrosine aminotransferase induction in somatic-cell hybrids.

Aryl hydrocarbon hydroxylase activity is inducible in mouse 3T3 fibroblasts by benz[alpha]anthracene, whereas no detectable basal or inducible levels of this enzyme occur in rat-hepatoma tissue culture cells. Conversely, tyrosine aminotransferase activity is inducible in hepatoma cells by dexamethasone, whereas only low noninducible levels of this enzyme exist in 3T3 cells. In hybrids formed by fusion of these two parent lines, levels of inducible hydroxylase activity range from the same as, to more than 20-fold greater than, that in the 3T3 parent; aminotransferase levels remain very low and noninducible in all of these same hybrids. A majority of the 1S-chromosomal complement from each parent is retained in most of these hybrids. The kinetics of hydroxylase induction and degradation, responses of hydroxylase induction to actinomycin D and cycloheximide, and the relative thermolability of the control and induced activities are similar in the 3T3 parent and in the hybrids. Failure to inactivate any of the aminotransferase activity in the hybrids with antibody specific for the rat enzyme indicates that all of the basal noninducible aminotransferase activity is derived from the mouse 3T3 parent.

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Microsomal hydroxylase induction in liver cell culture by phenobarbital, polycyclic hydrocarbons, and p,p'-DDT.

Aryl hydrocarbon hydroxylase induction by phenobarbital, polycyclic hydrocarbons, and the insecticide, 2.2-bis(p-chlorophenyl)-1,1,1-trichloroethane (p,p'-DDT), occurs in rat fetal liver cell cultures. The maximum net rate at which the hydroxylase activity accumulates is about the same when phenobarbital, 3-methlcholanthrene, or benz[a]anthracene is in the growth medium at optimum concentrations. An additive effect is obtained when either phenobarbital or p.p'-DDT is present with a polycyclic hydrocarbon in the growth medium, but not when the cells are treated with phenobarbital plus p.p'-DDT or with the combination of two polycyclic hydrocarbons.

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