Action of ASEA Redox Supplement on Stressed Cells

In this examination scientists evaluated the effects of ASEA Redox Supplement on cells that were stressed with cytokines (cachexin), radiation and serum starvation. Cytokines are cell signaling molecules that aid cell-tocell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection, and trauma.

Study Protocol

Cell cultures with normal random cell cycles and cultures approaching confluence received increasing concentrations of cachexin stressor (a group of proteins that can cause cell death). These cultures received either a pretreatment of 10% phosphate buffered saline solution control or 5 – 10% concentration of ASEA Redox Supplement for 24 hours. Researchers measured two indicators of cell viability: Serum LDH levels as an indication of membrane integrity and neutral red dye as a demonstration of lysosomal integrity. As cell membranes fail, LDH releases into the serum medium. Lower quantities of LDH indicate higher cell viability. The integrity of lysosomes, necessary for viable cell function, are measured by absorption of Neutral Red dye stain. Higher quantities of Neutral Red absorbance indicate higher cell viability.

Results Summary

The response of the cells, when stressed with cachexin, depends on upon cell phase. Normal random cycling cells exhibited a typical decrease in cell viability accompanied by cell death. Confluent end-of-life-cycle and borderline cells were less sensitive to cachexin insult, exhibiting less pronounced decreases in cell viability and less cell death. Exposure to ASEA Redox Supplement caused no significant change in the response of the normal random cycling cells to cachexin (showing a similar loss of cell viability and cell death). However, cultures approaching confluence exposed to ASEA Redox Supplement exhibited increased sensitivity to cachexin, restoring behavior comparable to that of normal cells. Borderline cells, exhibiting a relatively small cachexin response and confluent cells that are usually insensitive to cachexin insult exhibited a much stronger response to cachexin when exposed to ASEA Redox Supplement, both in a decrease in viability and increased cell death. It appears that exposure to ASEA Redox Supplement causes increased rates of confluent cell death, enhancing the natural reception of cachexin in end-oflife-cycle cells. Exposure to ASEA Redox Supplement is not expected to cause any change in normal cell viability. Cachexia is usually secreted to instigate cell death in damaged or dysfunctional tissues, allowing surrounding healthy cells to divide and fill in voids. Thus, increasing the sensitivity to cachexin in dysfunctional cells may help accelerate such a process and is not always considered harmful.

Acceleration of cell death in tissues stressed was seen with radiation and serum-starvation associated with exposure to ASEA Redox Supplement


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