this image shows lymphocytic toxicity.

this image shows that the buildup of dATP inhibits RNR (ribonucleotide reductase), which inhibits the rest dNTP synthesis.

bonus image shows RNR is the target of hydroxyurea.

If you just remembered the fact that RNR converts ribonucleotides to deoxyribonucleotides, it makes sense that excess dATP (a deoxyribonucleotide) would inhibit the enzyme

I did not know the mechanism of how dATP is harmful, although I knew that it was lymphotoxic. You can check out U world question ID: 15293 for a pretty good explanation

https://i.gyazo.com/af438e2d71c87b9c3e05ab802628526e.png

Got this wrong, but when looking this up, I saw that SCID is associated with a lack of adenosine deaminase --> accumulation of adenosine, which is lympho-toxic.

ADA def causes increase of dATP which strongly inhibits ribonucleotide reductase, reducing dNTP needed for DNA synthesis.

This would particularly effect lymphoid proliferation and function that relies heavily on nucleotide biosynthesis. Half of the cases of neonatal onset of SCID are due to ADA def.

So I missed this question and I was very confused at first as to why. When I first read this question, I thought of Cladribine. Cladribine (Hairy Cell Leukemia ttx) is an adenosine deaminase inhibitor. Cladribine inhibits DNA polymerase, and I chose DNA Polymerase I as my option. Why was I wrong?

Because DNA polymerase I is the prokaryotic DNA poly, not in human lymphocytes. I glanced over the "I" when I was taking this test. If you see this question on your exam, and DNA polymerase is an option - THATS the answer, but ribonucleotide reductase would be a more indirect inhibitor of DNA.

The question also asks for DNA synthesis specifically, which further suggests RR.

These NBMEs do be tricky.