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Physiologic apoptosis

The role of apoptosis in normal physiology is as significant as that of its counterpart, mitosis. It demonstrates a complementary but opposite role to mitosis and cell proliferation in the regulation of various cell populations. It is estimated that to [Pg.310]


Exposure to chemical compounds such as some heavy metals (e.g., lead) may activate apoptosis in a non-physiological way, leading to organ injury... [Pg.286]

In this type of reaction an antigen elicits the generation of cytotoxic T-lymphocytes ( immune defense). Cytotoxic T-lymphocytes (Tc) destroy antigen bearing cells by inducing apoptosis. This reaction can be viewed as the cellular counterpart to the humoral Type II reactions. They play an important physiological role in the defense of viruses, and can become allergic reactions under the same conditions as described for Type II reactions. [Pg.60]

Data about curcunfin encapsulated in liposomes have been reported recently. The authors encapsulated curcumin into a liposomal delivery system in order to study the in vitro and in vivo effects of this compound on proliferation, apoptosis, signaling, and angiogenesis using human pancreatic carcinoma cells. Carotenoids of different polarities and in competition with cholesterol were specifically incorporated into liposomes in order to mimic the physiological uptake by cells and monitor their antioxidant capacities. ... [Pg.316]

The water-soluble compound 36b, very stable within a physiological buffer at 37 ° C, exhibits cytotoxic effects on ovarian A2780 human cancer cells and promotes apoptosis to a greater extent than platinum drugs [103]. [Pg.68]

Hantz, H. L., L. F. Young, and K. R. Martin. 2005. Physiologically attainable concentrations of lycopene induce mitochondrial apoptosis in LNCaP human prostate cancer cells. Exp Biol Med (Maywood) 230(3) 171-179. [Pg.431]

In summary, unoxidized lycopene can act as a lipid and a DNA antioxidant at physiological concentrations but oxidized lycopene or high concentrations of lycopene, and depending upon the oxidizing conditions, may increase lipid peroxidation and oxidative DNA damage. Furthermore, the pro-oxidant effects may result in an increased apoptosis and a decreased cell viability, which should be kept in mind as studies on proliferation and apoptosis are reviewed. [Pg.445]

There are several alternative pathways associated with the balance between proliferation and apoptosis that are affected by lycopene treatment, especially the insulin-like growth factor (IGF) signaling pathway. Another is the possibility that lycopene or one of its breakdown products has retinoid activity. Kotake-Nara et al. compared acyclo-retinoic acid, an in vitro oxidation product of lycopene, to four actively researched anticarcinogenic retinoids. Acycloretinoic acid was found to more actively reduce PC-3 and DU-145 cell viabilities (but not LNCaP) through apoptosis in a medium already containing small amounts of natural retinoids. But study concentrations were 20 pM, far above physiologically relevant lycopene concentrations, let alone the smaller concentration of one of its breakdown products. Acycloretinoic acid had a very low affinity for the retinoid X receptors (RXR) and retinoic acid receptors (RAR) receptors (Kotake-Nara et al. 2002). [Pg.450]

Polunovsky, V. A., Rosenwald, I. B., Tan, A. T., White, J., Chiang, L., Sonenberg, N., and Bitterman, P. B. (1996). Translational control of programmed cell death Eukaryotic translation initiation factor 4E blocks apoptosis in growth-factor-restricted fibroblasts with physiologically expressed or deregulated Myc. Mol. Cell Biol. 16, 6573-6581. [Pg.331]

Skulachev [117] proposed that the released cytochrome c oxidizes superoxide and, by this, exhibits an antioxidant function. This proposal was supported by recent experimental findings by Atlante et al. [118], who suggested that cytochrome c released from mitochondria by oxygen species protected mitochondria through a feedback-like process oxidizing superoxide. The most important physiological inhibitor of apoptosis is multifunctional protein Bcl-2,... [Pg.757]

In conclusion, it should be stressed that the competition between pro- and antiapoptotic effects of nitric oxide must probably depends on its relevant levels [137] the low physiological levels of NO principally suppress the apoptotic pathway by several mechanisms, whereas the higher rates of NO production may overcome cellar protective mechanisms and stimulate apoptosis. Furthermore, the simultaneous formation of nitric oxide and superoxide increases the possibility of apoptosis activation due to the formation of peroxynitrite. [Pg.759]


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See also in sourсe #XX -- [ Pg.310 , Pg.311 ]




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Physiological mediator of apoptosis

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