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Biomedical subjects

E Bresnick

Publications and source records attributed to E Bresnick.

At least 145 records · Page 8Linked to original sources
PubMed1976

Aryl hydrocarbon hydroxylase in mouse mammary gland.

The specific activity of aryl hydrocarbon hydroxylase in the mammary gland has been measured in six different mouse strains comprising both mammary cancer susceptibility and resistance, under basal conditions, and after pretreatment of the mice with 3-methylcholanthrene (3MC). No correlation was observed between the ease of 3MC-enhanced mammary tumorigenesis and the basal or induced specific activity of aryl hydrocarbon hydroxylase. Furthermore, it was shown that in the AKR/J and A+/Ki mice, only minor enhancement in aryl hydrocarbon hydroxylase was seen upon injection of 3MC. The C57BL/6J and C3Hf/He Tex mammary glands responded the most in this regard. It was also shown that the inability of the AKR/J or A+/Ki mice to respond was not due to their inability to absorb 3MC from the peritoneal cavity and transmit the polycyclic hydrocarbon to the mammary gland.

Animals↗
PubMed1975

Increased translation as a result of elevated initation factor activity after administration of 3-methylcholanthrene.

Protein synthesis initiation factors present in a crude 0.5 M KCL microsomal wash fraction were isolated from the livers of immature rats that had been injected either 2 or 17 hours earlier with the plycyclic hydrocarbon, 3-methylcholanthrene (3MC), and then were tested for their ability to stimulate natural mRNA-directed protein synthesis in vitro. After purification of the initiation factors by means of ammonium sulfate fractionation, and DEAE-cellulose and Sephadex G-200 chromatography, M2A and M2B, but not M3 or M1, from the livers of 3MC-pretreated rats were more active than were similarly-prepared control factors in their ability to initiate the synthesis of rabbit globin polypeptides in a highly fractionated cell-free protein synthesizing system derived from rabbit reticulocytes. The greater activity of the M2A and M2B preparations from drug-treated rat liver did not appear to be due to differences in the composition of initiation factor protein extracted from the livers of control or experimental rats and occurred very early after administration of 3MC, i.e., 2 hr. The role of the protein synthesis initiation factors in the altered rates of protein synthesis which accompany cytodifferentiation and growth is discussed.

Ammonium Sulfate↗
PubMed1975

Simple vs. complex inheritance of inducible aryl hydrocarbon hydroxylase in mouse tissues.

The genetics of induction of hepatic and lung aryl hydrocarbon hydroxylase (AHH) have been studied in Af/Ki and AKR/Ki mice and in their F1 and F2 progeny after administration of 3-methylcholanthrene (3MC). Furthermore, the induction of AHH was investigated using the fetal liver explant model system with 3MC, trans-1,2-dihydroxy-3MC, and 4'-bromoflavone as the inducers. The results obtained with the above strains were contrasted with those from the C57BL/6Ki, DBA/2+Ki, and their crosses. The present investigation revealed a complex pattern of inheritance of basal and inducible AHH in lung and liver of AKR/Ki and Af/Ki, with a poor correlation between lung and liver. Hepatic AHH was not fully inducible in the F1 hybrids, while the frequency distribution function in the F2 mice was suggestive of more than two distinct classes.

Animals↗
PubMed1975

Histone modification in liver after administration of inducers of mixed function oxidase activity.

The phosphorylation and acetylation of rat liver histones in vivo were determined after administration of phenobarbital or 3-methylcholanthrene. No changes were observed in the phosphorylation profile of histones separated by gel electrophoresis after treatment with either of these two inducing agents. However, after 2h of treatment with either phenobarbital or 3-methylcholanthrene, a significant increase in acetylation of histones was noted, particularly in the F2a1 and (F3, F2b, F2a2) regions. It is suggested that this increase which precedes the enhancement in RNA synthesis may play a role in the alteration of transcription in liver.

Acetates↗
PubMed1975

Early morphologic alterations in mouse skin after topical application of 3-methylcholanthrene and its metabolites.

The effects of topical administration of 3-methylcholanthrene (MCA) or its metabolites on BALB/cKi mice were reported on inflammatory skin reactions, the alterations in epidermal thickness, the number of nucleated cells, pyknotic nuclei and/or nuclear fragments, and mitotic figures in the interfollicular epidermis (IFE). In the two-stage carcinogenesis system, MCA, the powerful complete carcinogen, induced an ordered sequence of cell changes strikingly similar to those caused by tumor-promoting agents such as the phorbol esters. These changes were absent after application of the "K-region" oxide of MCA. Other MCA metabolites also failed to induce notable inflammation, epidermal hyperplasia, and/or hypertrophy. Several MCA derivatives, however, caused a thinning of IFE paralleled by an increase in the relative number of pyknotic nuclei and a decrease in the total number of epithelial cells. The inhibitor of polycyclic hydrocarbon metabolism alpha-naphthoflavone did not prevent MCA-mediated skin reactions but, under suitable conditions, apparently potentiated the hyperplastic effects of MCA. The findings indicate that important events in the promotion phase of MCA-mediated skin carcinogenesis might be associated with the parent compound rather than with one of its metabolites.

Administration, Topical↗
PubMed1973

Gas chromatographic assay of epoxide hydrase activity with 3-methylcholanthrene-11,12-oxide.

Epoxide hydrase has been measured in rat tissue with 3-methylcholanthrene-11,12-oxide as substrate; diol formation was assayed by gas chromatographic separation of the trimethylsilylated derivative of trans-11,12-dlhydro-11,- 12-dihydroxy-3-methylcholanthrene from the corresponding derivative of the 11 (or 12)-hydroxy-3-methylcholanthrene on 3 percent OV-17, which is formed from the 11,12-oxide during the derivatization. The polycyclic hydrocarbons were extracted initially from the incubation mixture with ethyl acetate. The assay is simple, inexpensive, and sensitive.

Animals↗