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After degeneration of the intestinal external nerves capsaicin did not increase TK activity, suggesting the involvement of an axon reflex.
Exposing such "chronically" denervated intestinal segments to capsaicin did not significantly increase TK activity (102.7±3.1% of control; n = 5).
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Kaviraj and Sharma (2003) have noticed 10 and 5 % increased TK level during vermicomposting by E. fetida and Lampito mauritii, respectively.
Fourth, intra-arterial administration of the two peptides significantly increased TK activity (Figure 9).
Hence, exposing the intestinal mucosa to 1.6 mM capsaicin increased TK activity and 3H-thymidine incorporation into DNA reflecting events in crypt epithelial cells as confirmed by the BrdU experiments.
3′-deoxy-3′-[F]fluorothymidine uptake after 72 h of paclitaxel incubation was slightly increased, probably due to increased TK activity in these cells.
For 5-FU and paclitaxel, increased TK activity compared with untreated cells was found at 48 and 72 h, but these effects were minor.
It was hypothesized that increasing TK expression may enhance HSV-1 replication/gene expression thus promoting viral DNA replication and α expression during reactivation [ 47].
Although cells showed a G1 arrest (where TK-1 activity should be low), increased TK protein levels were found, but enzyme activity remained similar or increased much less compared with TK-1 levels in untreated cells.
In bladder cancer cells, TS inhibition results in both an increased TK activity and upregulated expression of the nucleotide transporter protein to maintain thymidylate levels through pyrimidine salvage (Pressacco et al, 1995).
Compared with untreated cells, 5-FU and doxorubicin increased TK-1 levels by >300.
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