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In this mini-review, we describe the previously reported yeast gene that contributes to SAM accumulation by overexpression, mutation or deletion and summarise the genetic approach for the production of SAM in large industrial quantities.

If our data based on an intense and short exposure to HNE can be extended to an in vivo situation where low concentrations of HNE are produced on a long time scale, the present results suggest that although the amount of DNA adducts is low upon treatment by exogenous HNE, their formation could be favored upon oxidative stress

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