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Biomedical subjects

S Yannai

Publications and source records attributed to S Yannai.

45 records · Page 3Linked to original sources
PubMed1983

Adrenocortical response to single and repeated doses of chloroform in rats.

The influence of single and repeated doses of chloroform on the adrenocortical function was studied in young male albino rats. One day after oral administration of a single dose of 1.5 g chloroform/kg body weight, adrenal hypertrophy developed and persisted for at least 12 days. The adrenal cholesterol content started to drop 3 h after the application, remained low for 1 day, then increased and remained elevated during the next 12 days. The plasma corticosterone content increased 15 min after the treatment and remained high during the next 4 h; 6 h after the treatment, when the anesthetic effects of CHCl3 had disappeared, it decreased somewhat; after 12 h it increased again, and the peak value was observed after 1 day. This was followed by a gradual drop, and after 8 days it reached the normal level. A second dose, administered 4 or 8 days after the first one, was still capable of stimulating the adrenocortical function. This was evidenced 24 and 48 h after the second dose. The response, however, was smaller than that observed after a single dose of the same stressor. The influence of a single dose of chloroform on corticosterone decay in the circulation 1 and 9 days after treatment, was tested in adrenalectomized rats injected with non-radioactive corticosterone, and in intact rats injected with 1,2-3H-corticosterone. Results for the adrenalectomized animals were inconclusive, whereas those for the intact ones proved that the treated animals metabolized corticosterone as well as the controls did.

Adrenal Cortex↗
PubMed1981

DNA-damaging agents and DNA-synthesis inhibitors induce luminescence in dark variants of luminous bacteria.

The DNA-damaging agents mitomycin C and UV irradiation, as well as the DNA-synthesis inhibitors nalidixic acid, novobiocin and coumermycin, induce the de novo synthesis of luciferase and in vivo luminescence in dark variant cells of the luminous bacteria Photobacterium leiognathi. Mitomycin C and nalidixic acid also cause the induction of luminescence in wild-type cells in the absence of its natural inducer. In spite of the high level of in vivo luminescence of the treated dark-variant cells, none of these agents result in the appearance of genetically luminous revertants. The possibility is discussed that these agents phenotypically induce luminescence through their ability to trigger 'SOS functions', which in turn leads to the transitory inactivation of certain repressors.

Aminocoumarins↗
PubMed1980

A new, sensitive and simple bioluminescence test for mutagenic compounds.

A spontaneous dark variant of the luminous bacterium Photobacterium leiognathi was isolated. The reversion frequency of this variant to genetic-hereditary luminescent cells is greatly increased by nanogram quantities of different base-substitution and frameshift agents. This makes it possible to detect mutagenic compounds at concentrations 100 times lower than that detected by the Ames Test. Curing agents, such as acridine dyes, ethidium bromide and sodium dodecyl sulfate, are also very active in the reversion of this dark variant to the luminous state, but fail to revert it to a genetic-hereditary luminescent type. The nature of the primary mutation in the dark variant, and the potential use of this luminescence system for detecting different classes of carcinogenic chemical, are discussed.

Drug Evaluation, Preclinical↗
PubMedDate not supplied

Induction of apoptosis in MCF-7 cells by indole-3-carbinol is independent of p53 and bax.

The anticancer activity of indole-3-carbinol and the possible mechanisms involved were explored in human breast cancer cell lines MCF-7 and T47D. Treatment with indole-3-carbinol suppressed the growth of MCF-7 and T47D cells. MCF-7 cells were more sensitive to indole-3-carbinol than T47D cells. The growth suppression caused by indole-3-carbinol was found to be partially involved in its ability to induce apoptosis (programmed cell death) in MCF-7 cells. Western blot analysis demonstrated that wild-type p53 was not induced after treatment of MCF-7 cells with indole-3-carbinol. Northern blot analysis showed that treatment of MCF-7 cells with indole-3-carbinol did not affect the expression of bax gene (one of the death genes). In the tissue culture medium, indole-3-carbinol was found to be partially converted to 3,3'-diindolylmethane. The experiments indicated that indole-3-carbinol suppressed MCF-7 cell growth in part by induction of apoptosis which was independent of p53 and bax expression and that the effect caused by indole-3-carbinol was partially due to its conversion to a more potent compound, 3,3'-diindolylmethane, in vitro.

Apoptosis↗