Apoptosis induction

MIYOSHI N, KOYAMA Y, KATSUNO Y, HAYAKAWA S, MITA T, OHTA T, KAJI K, ISEMURA M (2001) Apoptosis induction associated with cell cycle dysregulation by rice bran agglutinin. JBiochem, (Tokyo) 130 799-805. 

Nagase, M. Oto, J. Sugiyama, S. Yube, K. Takaishi, Y. Sakato, N. Apoptosis induction in HL-60 cells and inhibition of topoisomerase II by triterpene celastrol. Biosci. Biotechnol. Biochem. 2003, 67, 1883-1887. 

Hayakawa S, Saeki K, Sazuka M, et al. Apoptosis induction by epigallocatechin gallate involves its binding to Fas. Biochem Biophys Res Commun 2001 285 1102-1106. 

Another factor responsible for regulating the levels of p53 by (3-carotene could be the dose employed. At high carotenoid concentrations, an increase in p53 expression was observed in SCC cells (Schwartz, 1993) and in HL-60 cells (Palozza et al 2002b). In HL-60 cells, the treatment with the carotenoid induced a remarkable increase in ROS production, accompanied by an enhanced expression of p21WAFl and by a concomitant arrest of cell cycle at the G0/G1 phase (Palozza et al., 2002b). An arrest of cell cycle, accompanied by apoptosis induction, was also observed following dietary supplementation with lutein (Chew et al., 2003). The inhibition of mouse mammary tumor growth by lutein was also supported by the observed increase in the expression of p53 and Bax induced by the carotenoid (Chew et al., 2003). 

Herman-Antosiewicz A and Singh S V (2004), Signal transduction pathways leading to cell cycle arrest and apoptosis induction in cancer cells by Allium vegetable-derived organosulfur compounds a review , Mutation Res, 555, 121-131. 

Yang, G. et al. Apoptosis induction by the satratoxins and other trichothecene mycotoxins Relationship to ERK, p38 MAPK and SAPK/JNK Activation. Toxicol. Appl. Pharmacol. 164, 149-160, 2000. 

Byrd, J., Kitada, S., Flinn, L, Aron, J., Pearson, M., Lucas, D., and Reed, J.C., The mechanism of tumor cell clearance by rituximab leukemia evidence of caspase activation and apoptosis induction. Blood, 99, 1038-1043, 2002. 

In summary, the binding of oxLDL and/or lipids to several SC receptors (SRAI/II, CD36, CD68) has been clearly demonstrated. Most of other receptors may potentially bind oxLDL or lipids. Consequently, the cellular internalization of oxidized lipids by the SC receptor pathways may be involved in the biological effect of oxLDL, such as apoptosis induction. As a likely major ligand and because of their oxidized lipid contents, oxLDL may have many putative effects on different cells, such as alteration of cell signaling and gene expression. 

---