We examined how a selenium-containing drug, known as RuSe, targets cancer cells while sparing normal cells. This innovative approach leverages the unique properties of selenium, specifically its electrophilic center, to create oxidative stress within cancer cells. By shuttling electrons from biological electron donors, the drug activates a sequence of events detrimental to cancer survival.
The results were striking; we found that the rate of electron transfer at the selenium site is significantly higher in cancer cells compared to normal cells—1.81 times greater, to be precise. This selective action leads to a lethal effect, with the drug being 14.98 times more harmful to cancer cells than to their healthy counterparts. We observed that the generation of superoxide anions from this process causes DNA damage and triggers the p53 signaling pathway, which enhances the drug's effectiveness in killing cancer cells.
Our findings offer an exciting new avenue for crafting chemotherapeutic agents that can be both efficient and less toxic. By exploiting the special properties of selenium, we open the door to more intelligent and targeted cancer therapies that could reduce side effects for patients.
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