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Table 1.

Response of SR+ MCF-7 human breast cancer xenografts to perfusion in situ with a physiologic nocturnal concentration of melatonin

Treatment[3H]Thymidine incorporation (dpms/μg DNA)Linoleic acid uptake (% supply)13-HODE production (ng/min/g)cAMP (nmol/g)
Controls 47.4 ± 3.9 16.7 ± 1.7 0.97 ± 0.17 0.55 ± 0.11 
Melatonin 13.6 ± 1.6* 0.33 ± 0.12* 
Melatonin + 13-HODE 74.8 ± 6.3 333.17 ± 19.02 0.68 ± 0.06 
13-HODE 78.0 ± 6.5 17.2 ± 3.2 363.18 ± 10.62 0.78 ± 0.17 
Treatment[3H]Thymidine incorporation (dpms/μg DNA)Linoleic acid uptake (% supply)13-HODE production (ng/min/g)cAMP (nmol/g)
Controls 47.4 ± 3.9 16.7 ± 1.7 0.97 ± 0.17 0.55 ± 0.11 
Melatonin 13.6 ± 1.6* 0.33 ± 0.12* 
Melatonin + 13-HODE 74.8 ± 6.3 333.17 ± 19.02 0.68 ± 0.06 
13-HODE 78.0 ± 6.5 17.2 ± 3.2 363.18 ± 10.62 0.78 ± 0.17 

NOTE: Effects of perfusion of tissue-isolated SR+ MCF-7 human breast cancer xenografts in situ with synthetic melatonin (1 nmol/L) in the presence or absence of 13-HODE (12 μg/mL) on [3H]thymidine incorporation into DNA, linoleic acid uptake, 13-HODE formation, and cAMP levels. Individual tumors (n = 3-4) were perfused over a 2-hour period (06:30 to 08:30 h) with whole blood collected from tumor-free donor rats during the early light phase when endogenous melatonin levels were low. Synthetic melatonin and 13-HODE were added to the whole-blood perfusate to achieve final concentrations of 1 nmol/L (232 pg/mL) and 12 μg/mL, respectively. Values are means ± SE.

*

P < 0.05 vs controls and melatonin + 13-HODE (comparisons of relevance).

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