Submitted to: American Society of Biochemists and Molecular Biologists
Publication Type: Abstract Only
Publication Acceptance Date: March 31, 1996
Publication Date: N/A
Technical Abstract: Normal sexual development in males of many species is dependent upon adequate dietary Zn. One effect of Zn deficiency during development in rats is reduced testicular ACE activity (Reeves and Rossow, PSEBM, 203:336, 1993). ACE concentration is reduced in both sperm and germ cells (Reeves and Stallard, J Tr Elem Exp Med, 7:125, 1995). The present study was undertaken to determine if the change in ACE concentration were caused by reduced transcription of the ACE gene and to follow the effect of the Zn-deficiency over time. Young adult male rats were placed in one of three feeding regimens for up to 7 weeks: 1) Zn adequate diet, 35 mg Zn/kg, fed ad libitum (+ZnAL); 2) Zn deficient diet, <1 mg Zn/kg, fed ad libitum (- ZnAL); 3) Zn adequate diet pair fed to the deficient group (+ZnPF). Five animals from each group were killed after 3, 5, and 7 weeks on the dietary regimen. Zn deficiency was confirmed in -ZnAL by reduced serum Zn concentrations. After 3 weeks, testicular ACE activity in -ZnAL was only 50% that of either +Zn group. After 5 weeks, ACE activity in -ZnAL fell to 5% of control values and remained so after 7 weeks. Northern blots of testicular RNA were used to compare the 3 dietary regimens at each period, and hybridized separately with 2 cDNA probes: ACE.5 and G3PDH. Autoradiographs revealed that the amount of ACE mRNA in -ZnAL after 5 and 7 weeks was reduced compared to either +Zn group. Densitometric analysis comparing peak area and peak height showed that ACE/G3PDH ratios were reduced to 33% the value for +ZnAL and to only 20% that of +ZnPF. Thus, the results suggest that the reduction in ACE concentration in testes of Zn deprived rats is caused by a reduction in transcription of the ACE gene rather than reduced translation.