Apoptosis, stress-induced

It has been shown in many studies that protective effects of carotenoids can be observed only at small carotenoid concentrations, whereas at high concentrations carotenoids exert pro-oxidant effects via propagation of free radical damage (Chucair et al., 2007 Lowe et al., 1999 Palozza, 1998, 2001 Young and Lowe, 2001). For example, supplementation of rat retinal photoreceptors with small concentrations of lutein and zeaxanthin reduces apoptosis in photoreceptors, preserves mitochondrial potential, and prevents cytochrome c release from mitochondria subjected to oxidative stress induced by paraquat or hydrogen peroxide (Chucair et al., 2007). However, this protective effect has been observed only at low concentrations of xanthophylls, of 0.14 and 0.17 pM for lutein and zeaxanthin, respectively. Higher concentrations of carotenoids have led to deleterious effects (Chucair et al., 2007). 

Mukherjee, PK, Marcheselli, VL, de Rivero Vaccari, JC, Gordon, WC, Jackson, FE, and Bazan, NG, 2007. Photoreceptor outer segment phagocytosis attenuates oxidative stress-induced apoptosis with concomitant neuroprotectin D1 synthesis. Proc Natl Acad Sci U SA 104, 13158-13163. 

Monti D, Moretti L, Salvioli S, Straface E, Malorni W, Pellicciari R, Schettini G, Bisaglia M, Pincelli C, Fumelli C, Bonafe M, Franceschi C (2000) C60 carboxyfullerene exerts a protective activity against oxidative stress-induced apoptosis in human peripheral blood mononuclear cells. Biochemical and Biophysical Research Communications 277 711-717. 

Antonsson and Marinou 2000 Adams and Cory, 1998). Stress may also cause inaease, nitric oxide (NO), or reactive oxygen species (ROS) production which, in turn, triggers release of apoptotic proteins from the intermemhrane space (Kroemer and Reed, 2000 Vieira et at, 2000). Release of these proteins from mitochondria are required for stress induced killing hut are, with a few exceptions (Bergmann et al, 1994, Schulze- Osthoff et al, 1993), dispensible for CD95 and TNF-receptor transduced apoptosis. These other death processes require FADD and caspase-8 to be recruited into the death receptor complexes and cannot be blocked by Bcl-2 (Krammer, 2000 Scaffidi et al, 1998). 

Williams, R.S., 2000, Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis. Cell 101 389-399. 

Figure 3. The many ways to lose a HAT. Decreased amounts of functional CBP protein and subsequent CBP s loss of function has been observed in different contexts of neurological disorders and neuronal apoptosis. RTS (Rubinstein-Taybi Syndrome) results from a mutation on one cbp gene allele. In several cases of polyQ diseases, CBP can be sequestred by the mutated polyQ proteins, forming aggregates in the cytoplasm or the nucleus. CBP proteasomal degradation was also shown to be favored by polyQ proteins. CBP is a caspase-6 substrate in cerebellar granule neurons (CGN) deprived of potassium modeling caspase-dependent apoptosis. Finally, cbp gene repression has been observed in oxidative stress-induced death of a motomeuronal cell line. The mechanisms by which CBP levels are reduced in motomeurons of ALS mice is still unknown...

C. L. Crowley-Weber, K. Dvorakova, C. Crowley, H. Bernstein, C. Bernstein, H. Garewal and C. M. Payne, Nicotine increases oxidative stress, activates NF-kappaB and GRP78, induces apoptosis and sensitizes cells to genotoxic/xenobiotic stresses by a multiple stress inducer, deoxy-cholate relevance to colon carcinogenesis, Chem. Biol. Interact., 2003, 145(1), 53. 

Since flavonoids are able to bind to the BDZ binding site of the GABA-A receptor, they might well interact with the BDZ binding site of the mitochondrial permeability transition protein, thereby modulating oxidative stress-induced apoptosis. ... 

There is a common feature in the two major neurodegenerative diseases In both Alzheimer s disease (AD) and Parkinson s disease (PD) there is an imbalance of metal metabolism leading to oxidative stress-induced neuronal apoptosis. It is well known that there is no cure or efficient treatment available for these diseases. Is there a way to prevent these diseases From this review... 

Ratan R. R., Murphy T. H., and Baraban J. M. (1994). Oxidative stress induces apoptosis in embryonic cortical neurons. J. Neurochem. 62 376-379. 

Mathai, J.P., Germain, M., and Shore, G. C., 2005, BH3-only BIK regulates BAX,BAK-dependent release of Ca2+ from endoplasmic reticulum stores and mitochondrial apoptosis during stress-induced cell death, J. Biol. Chem. 280, pp. 23829—23836... 

Mattson, M. P., Goodman, Y., Luo, H., Fu, W., and Furukawa, K. (1997). Activation of NF-kappaB protects hippocampal neurons against oxidative stress-induced apoptosis Evidence for induction of manganese superoxide dismutase and suppression of peroxynitrite production and protein tyrosine nitration.. Neurosci. Res. 49, 681-697. 

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