Inhibition and enhancement of skin tumors in mice by dimethyl sulfoxide depending on method of application.

The role of dimethyl sulfoxide [(DMSO) CAS: 67-68-5] in experimental tumorigenesis was investigated because of conflicting reports in the literature ranging from inhibition to no effect to enhancement. With the use of numbers of skin tumors produced on the back of the mouse following topical applications of carcinogenic agents as the variable and with acetone serving as the control solvent, the following results were obtained: When DMSO was the solvent for benzo[a]pyrene (CAS: 50-32-8) in the single-stage model (C3H mice), tumor numbers doubled. When DMSO was the solvent for 7,12-dimethylbenz[a]anthracene (CAS: 57-97-6) serving as initiator in the two-stage model (CD-1 mice), tumor numbers were unaffected. In the two-stage model, when DMSO was the solvent for the potent promoter phorbol-12-myristate-13-acetate [(PMA) CAS: 16561-29-8] or was applied to skin at the initiation site (the back) before PMA, tumor numbers were reduced to one-third of control. However, when DMSO was applied before PMA to the abdomen, a site remote from initiation, tumor numbers doubled. Enhancement of PMA appears to be unique. Recognition that diverse effects can occur depending on the method of application of DMSO may help to decipher the conflicting literature on its relation to tumorigenesis, could be of value in probing the mechanism of tumor promotion, and might signal further caution in its clinical use.