The Interplay between Autophagy and Aging

Numerous studies have established a link between autophagy and aging; however, the relationship has not been clearly defined. Aging is a very complex process caused by the accumulation of various factors due to the gradual failure of cellular maintenance. Recent studies have shown that autophagy reduces the stress responses induced by starvation, reactive oxygen species, and the accumulation of intracellular proteins and organelles through cytoprotection, clearance of damaged mitochondria, and lysosomal degradation. Here, we summarize our current understanding of the relationship between autophagy and the aging process.

The Interplay between Autophagy and Aging

Numerous studies have established a link between autophagy and aging; however, the relationship has not been clearly defined. Aging is a very complex process caused by the accumulation of various factors due to the gradual failure of cellular maintenance. Recent studies have shown that autophagy reduces the stress responses induced by starvation, reactive oxygen species, and the accumulation of intracellular proteins and organelles through cytoprotection, clearance of damaged mitochondria, and lysosomal degradation. Here, we summarize our current understanding of the relationship between autophagy and the aging process.

Molecules and their functions in autophagy

Autophagy is a self-degradation system of cellular components through an autophagosomal-lysosomal pathway. Over the last 15 yr, yeast genetic screens led to the identification of a number of genes involved in the autophagic pathway. Most of these autophagy genes are present in higher eukaryotes and regulate autophagy process for cell survival and homeostasis. Significant progress has recently been made to better understand the molecular mechanisms of the autophagy machinery. Especially, autophagy process, including the regulation of autophagy induction through mTOR and the nucleation and elongation in autophagosome formation through class III phosphatidylinositol 3-kinase complex and ubiquitin-like conjugation systems, became evident. While many unanswered questions remain to be answered, here, we summarize the recent process of autophagy with emphasis on molecules and their protein complexes along with advanced molecular mechanisms that regulate the autophagy machinery.

Study of Capsaicin-induced Apoptosis in Human Colon Cancer Cell Lines

PURPOSE: Numerous investigations have been conducted in order to determine the potential carcinogenic or chemopreventive activity of capsaicin. The aim of this study is to characterize the effects of capsaicin on colon cancer cells, and provide valuable information concerning the application of capsaicin in chemoprevention as well as for therapeutic purposes. METHODS: CoLo320DM and LoVo cells (human colon cancer cell line) were treated with capsaicin. In order to access cell viability and altered morphology, an MTT assay was performed and the cells were microscopically examined. Decreasing DNA staining was accessed by FACS. The cells were stained with FITC labeled annexin V and analyzed by FACS to detect cellular membrane alteration during apoptosis. The cells were stained with DiOC6(3) and Hydroethidine and analyzed by FACS in order to access ROS and dleta psi m. RESULTS: Capsaicin decreased cell viability in a dose-dependent manner. Capsaicin produced a cell morphology corresponding to the apoptotic features including cell shrinkage and chromatic condensation. Capsaicin treated cells induced a loss of nuclear DNA leading to hypoploidy in a dose-dependent manner. Cells were excluded by double staining with PI and FITC labeled annexin v and detected by FACS. We show that treatment of CoLo320DM, L0Vo cells with increasing concentrations of capsaicin parallel an increase in the percentage of red fluorescent cells (HE-->Eth) that reflect ROS hypergeneration and a decrease in the percentage of green fluorescent cells that reflect delta psi m disruption. CONCLUSION: These results clearly demonstrate that capsaicin-induced colon cancer cell death is apoptotic.