Effect of thyroxine, testosterone, and corticosterone on nerve growth factor (NGF) and epidermal growth factor (EGF) concentrations in adult female mouse submaxillary gland: dissociation of NGF and EGF responses.

Abstract

Testosterone propionate (TP) and corticosterone acetate (CA) were administered alone and in combination with T4 to assess the effect on submaxillary gland (SMG) nerve growth factor (NGF) and epidermal growth factor (EGF) concentrations in adult female mice. Mice were treated for 5 or 10 days. SMG NGF, and EGF concentrations were measured by specific RIA techniques. Mean SMG NGF (0.68 +/- 0.08 microgram/mg protein) and EGF (0.58 +/- 0.05 microgram/mg protein) concentrations were similar in control mice. T4 (0.4 microgram/g BW, sc, daily) significantly increased mean SMG NGF and EGF concentrations to 469% and 347%, respectively, of control values after 5 days and to 1190% and 568%, respectively, after 10 days of treatment. TP (25 microgram/g BW, sc, every 2 days) significantly increased mean SMG NGF and EGF concentrations to 734% and 767%, respectively, of control values at 5 days and to 1971% and 1953%, respectively, at 10 days. T4 and TP resulted in no further significant increases in either SMG NGF or EGF concentrations above the levels observed after TP alone. CA (25 microgram/g BW, sc, daily) increased mean SMG NGF, but not EGF, concentrations at both 5 and 10 days. Moreover, T4 and CA appeared to exert an additive effect on NGF. In contrast to the observations in adult female mice, T4 increased mean SMG NGF concentrations to 178% of control levels in adult male mice, but had no significant effect of SMG EGF concentrations. These data indicate that T4 and TP modulate SMG NGF and EGF concentrations in adult female mice. T4, however, appears to have a preferential effect on NGF on both male and female mice, unlike the equal effect on TP on both NGF and EGF. CA, like T4, also appears to increase NGF, but not EGF, concentrations in adult female SMG. The present results suggest separate regulatory mechanisms for T4, TP, and CA on SMG NGF and EGF biosyntheses.