The Implication of Low Dose Dimethyl Sulfoxide on Mitochondrial Function and Oxidative Damage in Cultured Cardiac and Cancer Cells

Area of Science:

• Cell Biology
• Biochemistry
• Toxicology

Background:

• Dimethyl sulfoxide (DMSO) is widely used, but its effects at low, "non-toxic" doses on cardiac and cancer cells remain unclear.
• Understanding DMSO's impact on cellular respiration, viability, and apoptosis is crucial for its safe application.

Purpose of the Study:

• To investigate the direct effects of varying low dimethyl sulfoxide (DMSO) concentrations on H9c2 cardiomyoblasts and MCF-7 breast cancer cells.
• To elucidate the dose-dependent impact of DMSO on cellular bioenergetics, oxidative stress, and apoptosis in these cell types.

Main Methods:

• H9c2 cardiomyoblasts and MCF-7 breast cancer cells were exposed to DMSO concentrations ranging from 0.001% to 3.7% for 6 days.
• Cellular respiratory control ratio, viability, maximal respiratory capacity, ATP-linked respiration, and apoptosis rates were assessed.

Main Results:

• DMSO doses below 0.5% enhanced cardiomyoblast respiratory control and viability, while 3.7% induced apoptosis via mitochondrial dysfunction and oxidative stress.
• In cancer cells, DMSO (≥0.009%) reduced maximal respiration and ATP-linked respiration, increasing ROS production and apoptosis.
• A surprising finding was that 0.001% DMSO significantly increased cancer cell proliferation.

Conclusions:

• DMSO exhibits differential effects on cardiac and cancer cells, with low doses showing potential benefits for cardiomyoblasts but risks for cancer cells.
• The study highlights the need for caution when using DMSO in cancer research and therapy due to its complex effects on cell proliferation and bioenergetics.
• DMSO's paradoxical effects underscore the importance of precise dose control and cell-type specific evaluation in biological applications.