Mitotic activity, suppression

Suppression of mitotic activity Trichlorfon, carbaiyl, thiram, nitro-aldicarb... 

Mechanism of Action A topical corticosteroid that inhibits accumulation of inflammatory cells at inflammation sites, suppresses mitotic activity, and causes vasoconstriction. Therapeutic Effect Decreases or prevents tissue response to inflammatory process. 

Cameron, I.L., Ord, V.A., Hunter, K.E., Padilla, G.M. Heitman, D.W. (1989) Suppression of a carcinogen (1,2-dimethylhydrazine dihydrochloride)-induced increase in mitotic activity in the colonic crypts of rats by addition of dietary cellulose. Cancer Res., 49, 991-995... 

Koizumi A, Tsukada M, Wada Y, Masuda H, Weindruch R. Mitotic activity in mice is suppressed by energy restriction-induced torpor. J Nutr 1992 122 1446-1453. 

H- Sabe, A. Hata, M. Okada, H. Nakagawa, and H. Hanafusa. Analysis of the binding of the Src homology 2 domain of Csk to tyrosine-phosphorylated proteins in the suppression and mitotic activation of c-Stc. Proc Natl Acad Sci, USA, 91 (9), 3984-3988, 1994. 

Many PAs and SPRMs display antiproliferative effects in the nonhuman primate endometrium where they suppress estrogen-dependent endometrial proliferation and mitotic activity, secretory activity, and reduce endometrial thickness and wet weight [31, 32]. This antiproliferative effect has been described as noncompetitive [31]. 

Any model for the biochemical oscillator controlling the onset of mitosis should account for the fact that, in some cells or at certain stages of development, mitosis can be prevented and cells cease to divide. In dynamic terms, such a transient or permanent suppression of mitotic activity can be viewed as a switch of the mitotic control system from an oscillatory into a nonoscillatory regime corresponding to a stable steady state. Models for the mitotic oscillator allow the discussion of possible mechanisms whereby the mitotic clock might be arrested. 

It should be emphasized that the time between the beginning of the treatment and the appearance of the aberrations in anaphase (or metaphase) can be used as an indicator of the stage affected only when the mitotic activity is not markedly suppressed by the treatment. The longer the period between treatment and fixation, the less accurate is the time method. An accurate determination of stage sensitivity in root tips can be obtained only by using cells labeled at a particular stage of the mitotic cycle (for methods of labeling, see Kihlman, 1966). 

Within 8 h after application of a single therapeutic dose of I, the mitotic index markedly decreased from 33%c (control value) to %> (Fig. 32). Mitotic activity remained suppressed, no signs of revival were detectable during the following days. 

As the count the nuclei in the seedlings after treatment by phosphemid at concentrations of 1 x 10 to 5 x 10 Mof 68 500 counted nuclei were 743 metaphases, an average of 1.08 0.06%, thus phosphemid suppressed mitotic activity more than twice (see above 2.82% in control). 

Vinblastine is an alkaloid derived from the periwinkle plant Vinca rosea. Its mechanism of action involves inhibition of tubulin polymerization, which disrupts assembly of microtubules, an important part of the cytoskeleton and the mitotic spindle. This inhibitory effect results in mitotic arrest in metaphase, bringing cell division to a halt, which then leads to cell death. Vinblastine and other vinca alkaloids are metabolized by the liver P450 system, and the majority of the drug is excreted in feces via the biliary system. As such, dose modification is required in the setting of liver dysfunction. The main adverse effects are outlined in Table 54-4, and they include nausea and vomiting, bone marrow suppression, and alopecia. This agent is also a potent vesicant, and care must be taken in its administration. It has clinical activity in the treatment of Hodgkin s... 

As a whole, the results presented above indicate that low concentrations of Vinca alkaloids, probably similar to therapeutic concentrations, have an antiproliferative activity that is due to inhibition of mitotic spindle function by changing the dynamics of microtubules rather than by depolymerizing them. A growing body of evidence seems to indicate that, specially in cancer cells, where mitosis regulation is already disrupted, the suppression of microtubule dynamics with mitosis arrest induces a signaling cascade leading to cell death by apoptosis (a type of programmed cell death) [172-174]. 

Tea polyphenols exhibit a variety of biological properties, including antioxidative effects [6], inhibition of extracellular mitotic signals [7], inhibition of cell cycle at the G1 phase [8], suppression of inducible nitric oxide synthase (iNOS) [7, 9], and induction of apoptosis in cancer cells [10]. The natural history of carcinogenesis and cancer provides a strong rationale for a preventive approach to the control of this disease and leads to considerations of the possibility of active pharmacological intervention, or chemoprevention, to arrest or reverse the carcinogenesis prior to invasion and metastasis [11. 12]. 

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