The aim of this study was to explore whether or not acetylresveratrol as a potential substitute for resveratrol dragged the toxic aldehyde to inhibit the mutation of mitochondrial DNA. The results revealed that the acetylresveratrol shifted ultraviolet peak of trans-crotonaldehyde from 316 to 311 nm. In mitochondria, the acetylresveratrol split the ultraviolet peak at 311 nm of trans-crotonaldehyde into 311 nm and 309 nm; the aldehyde Raman band of trans-crotonaldehyde was red shifted by the acetylresveratrol from 1689 to 1686 cm(-1) with obvious band decline; Raman bands at 1149 cm(-1), 1168 cm(-1), and 1325 cm(-1) of acetylresveratrol disappeared. In aldehyde dehydrogenase, the aldehyde Raman band of trans-crotonaldehyde was red shifted by the acetylresveratrol from 1689 to 1684 cm(-1) with band decline; Raman bands at 1150 cm(-1), 1168 cm(-1), and 1324 cm(-1) of acetylresveratrol declined. The weak acidic microenvironment was the best, for the acetylresveratrol dragged the toxic aldehyde of trans-crotonaldehyde. Compared with the resveratrol, the effect of the acetylresveratrol on the toxic aldehyde of trans-crotonaldehyde was very similar to that of the resveratrol. The acetylresveratrol is very suitable as a potential substitute for resveratrol dragged the toxic aldehyde to inhibit the mutation of mitochondrial DNA. Graphical In mitochondria, the Raman band of the toxic -CH=O of trans-crotonaldehyde (TCA) dragged by the Acetyl-Res from 1689 to 1686 cm(-1) with obvious band decline, while the Raman bands at 1149 cm(-1), 1168 cm(-1), and 1325 cm(-1) of the Acetyl-Res disappeared, respectively. The Acetyl-Res is very suitable as a potential substitute, for the Res dragged the toxic -CH=O of TCA to inhibit the mutation of mitochondrial DNA for anticancer.