Thymidine

The Cordyceps sinensis

In vitro assessment of 2-fluoro-2-deoxy-D-glucose, L-methionine and thymidine as agents to monitor the early response of a human adenocarcinoma cell line to radiotherapy.[Pubmed:8478710]

J Nucl Med. 1993 May;34(5):773-9.

The tumor cell uptake of three tracers that can be labeled with isotopes suitable for PET imaging--FDG, L-methionine and Thymidine--were examined in vitro in a human ovarian carcinoma cell line (HTB77IP3) at varying times following 30 Gy 60Co irradiation and were compared to a nonirradiated control group. FDG, methionine and Thymidine uptake per tissue culture well all increased following irradiation when compared to basal values, although to a much lower extent than the increases in uptake seen in a nonirradiated group. This increase in tracer uptake occurred despite a 6.25-fold decline in viable cell numbers. When examined per cell, FDG uptake per cell increased 9.77-fold, methionine 7.82-fold and Thymidine 9.48-fold over basal levels from Day 0 to Day 12 following irradiation. Part of these increases may be due to giant cell formation and/or radiation repair processes that require energy, protein and DNA substrates. While the in vitro system differs from in vivo systems due to the absence of a blood supply in vitro, a lack of infiltrating leukocytes and other factors, our data suggest that early assessment of human adenocarcinoma response to radiotherapy by PET with these tracers may be complicated by this normal increase in tracer uptake postirradiation. Clearly, in this human cancer cell line, early radiation-induced cell death is not associated with an early decline in tumor cell uptake of FDG, methionine or Thymidine.

Thymidine kinase 2 enzyme kinetics elucidate the mechanism of thymidine-induced mitochondrial DNA depletion.[Pubmed:25215937]

Biochemistry. 2014 Oct 7;53(39):6142-50.

Mitochondrial Thymidine kinase 2 (TK2) is a nuclear gene-encoded protein, synthesized in the cytosol and subsequently translocated into the mitochondrial matrix, where it catalyzes the phosphorylation of Thymidine (dT) and deoxycytidine (dC). The kinetics of dT phosphorylation exhibits negative cooperativity, but dC phosphorylation follows hyperbolic Michaelis-Menten kinetics. The two substrates compete with each other in that dT is a competitive inhibitor of dC phosphorylation, while dC acts as a noncompetitive inhibitor of dT phosphorylation. In addition, TK2 is feedback inhibited by dTTP and dCTP. TK2 also phosphorylates a number of pyrimidine nucleoside analogues used in antiviral and anticancer therapy and thus plays an important role in mitochondrial toxicities caused by nucleoside analogues. Deficiency in TK2 activity due to genetic alterations causes devastating mitochondrial diseases, which are characterized by mitochondrial DNA (mtDNA) depletion or multiple deletions in the affected tissues. Severe TK2 deficiency is associated with early-onset fatal mitochondrial DNA depletion syndrome, while less severe deficiencies result in late-onset phenotypes. In this review, studies of the enzyme kinetic behavior of TK2 enzyme variants are used to explain the mechanism of mtDNA depletion caused by TK2 mutations, Thymidine overload due to Thymidine phosphorylase deficiency, and mitochondrial toxicity caused by antiviral Thymidine analogues.

Thymidine, a specific precursor of deoxyribonucleic acid, is used as a cell synchronizing agent. Thymidine is a DNA synthesis inhibitor that can arrest cell at G1/S boundary, prior to DNA replication.

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