DNA strand breaks

Bleomycin acts by induction of DNA strand breaks.

Experimental evidence has suggested that every BLM molecule induces an average of 8 to 10 DNA strand breaks.

The main function of radiotherapy is to produce DNA strand breaks, causing severe DNA damage and leading to cell death.

These ROS may result in the production of many base adducts, as well as DNA strand breaks and crosslinks.

PARPs are enzymes that are activated by DNA strand breaks and play a role in DNA base excision repair.

Lithocholic acid has been shown to produce DNA strand breaks and both chenodeoxycholic acid and lithocholic acid induce mitotic aneuploidy in yeast cells.

However, treatment with Top1 inhibitors, such as the camptothecins, stabilize the cleavable complexes, prevent DNA religation and induce lethal DNA strand breaks.

Niacinamide also inhibits poly(ADP-ribose) polymerases (PARP-1), enzymes involved in the rejoining of DNA strand breaks induced by radiation or chemotherapy.

Although this study demonstrated that the flavonolignans of Silybum marianum (L.) are capable of inhibiting cellular proliferation and inducing DNA strand breaks, the results were obtained at very high concentrations that may be difficult to achieve in humans.