Modulation by cellular cholesterol of gene transcription via the cyclic AMP response element.

The effect of rapid changes in cellular cholesterol content on adenosine 3',5'-cyclic monophosphate (cAMP) response element-mediated gene transcription was investigated. The study was carried out in Chinese hamster ovary (CHO-K1) cells permanently expressing the human beta(2)-adrenoceptor. Gene transcription was quantified using a reporter gene (secreted placental alkaline phosphatase) under the transcriptional control of cAMP response element (CRE) sequences.

Evaluation of the V79 cell metabolic co-operation assay as a screen in vitro for developmental toxicants.

Inhibition of intercellular communication is proposed to be one of several possible mechanisms of teratogenesis. 38 coded compounds were tested for their effect on intercellular communication in the V79 cell metabolic co-operation assay. Test chemicals were selected from a list of 47 agents recommended for the evaluation of assays in vitro for developmental toxicants.

Inhibition of intercellular communication in Chinese hamster V79 cells by fractionated asphalt fume condensates.

Asphalt fume condensate is a skin carcinogen in mice, yet this complex mixture contains relatively low levels of known carcinogenic initiators. Consequently, its biological activity has been attributed to the presence of cocarcinogenic or tumor-promoting agents. One of several proposed mechanisms of tumor promotion is inhibition of intercellular communication.

Reactivity of catecholamines and related substances in the mouse lymphoma L5178Y cell assay for mutagens.

Using the L5178Y mouse lymphoma cell thymidine kinase locus and the Salmonella his locus assays, the mutagenic potentials of several catecholamines and related compounds were examined. No supplementary metabolic activation systems were used. In the mouse lymphoma assay, the dihydroxybenzenes catechol and hydroquinone had similar and appreciable mutagenic potentials, whereas resorcinol was less active.