Cells with high rates of proliferation are more susceptible to DNA damage. For instance, embryonic stem cells (ESCs) are known to be very sensitive to DNA damage and undergo rapid apoptosis even after low damage doses. Human embryonic stem cells (hESCs) show an atypical cell cycle regulation characterized by a high proliferation rate and a short G1-phase. The shortened G1-phase might protect ESCs from external signals inducing differentiation.
The DNA damage sensitivity in hESCs has been shown to correlate with a cell-intrinsic property termed as mitochondrial priming. Mitochondrial readiness for apoptosis is known as mitochondrial priming. Specifically, the balance between proapoptotic and antiapoptotic proteins is shifted closer to the apoptotic threshold in the case of hESCs.
I have attached a few articles below for your reference.
Article A High Proliferation Rate Is Required for Cell Reprogramming...
Article Stem cells: Balancing resistance and sensitivity to DNA damage
Article High Mitochondrial Priming Sensitizes hESCs to DNA-Damage-In...
Article Human Embryonic Stem Cells Have Constitutively Active Bax at...
It depends on the type of DNA damage you are inflicting/assaying for; many cancer cell lines have impaired (or absent) repair of a specific type of DNA lesion. Therefore cells lacking that lack that a specific repair function are super sensitive to agents that cause that specific lesion in high yield. Thus cells which lack MGMT are super sensitive to guanine O-6 alkylators etc.
Since, the cell lines Dr. Vijay K. Bharti lists aren't cancer cell lines with known defects in DNA repair, and likely just respond to significant DNA damage by undergoing apoptosis, I would decide what kind of DNA damage I wanted (e.g., GC base pair replaced by AT) and pick an agent that caused this change (e.g., MNNG in this case).