RESUMO
We found previously that Ac-(Leu-Leu-Ala-Arg-Leu)3-NHCH3 (5(3)), a model of the extension peptide of cytochrome P-450(SCC) precursor, strongly inhibited the import of the precursor into mitochondria. Unexpectedly, however, 5(3) showed the break of respiratory control of mitochondria. In the present study, desAc- [Pro7, Ser10] 5(3) (1), [Pro7, Ser10] 5(3) (2), desAc- [Gly5, Pro7, Ser10] 5(3) (3) and [Gly5, Pro7, Ser10] 5(3) (4) were synthesized in order to investigate the influence of the Gly, Pro and Ser residues, which are present in the extension peptide, on the import and respiration. CD measurement indicated that all the peptides had an alpha-helical conformation in the presence of DPPC-DPPG (3:1) liposomes. The order of the content of alpha-helical conformation was 5(3) greater than 1, 2 greater than 3, 4, while SEP1-15 (N-terminal 1-15 fragment of the extension peptide of cytochrome P-450(SCC) precursor) showed no alpha-helical structure. The measurements of dye-leakage from liposomes, import-inhibition of P-450(SCC) and adrenodoxin precursors and respiratory inhibition of mitochondria indicated that 3 and 4, rather than 1 and 2, are similar to SEP1-15, and that the glycine residue in the extension peptide is of considerable importance for the import of the precursors.
Assuntos
Bactérias/efeitos dos fármacos , Glicina , Mitocôndrias Hepáticas/metabolismo , Peptídeos/farmacologia , Prolina , Serina , Sequência de Aminoácidos , Animais , Antibacterianos/farmacologia , Bactérias/crescimento & desenvolvimento , Dicroísmo Circular , Testes de Sensibilidade Microbiana , Mitocôndrias Hepáticas/efeitos dos fármacos , Dados de Sequência Molecular , Consumo de Oxigênio/efeitos dos fármacos , Peptídeos/síntese química , Conformação Proteica , RatosRESUMO
In the present study, we demonstrated that hypertensive left ventricular hypertrophy can be divided angiographically into symmetrical (SH) and asymmetrical septal hypertrophy (ASH) groups. In the SH group, the dynamics of the septal wall and the free wall were almost the same as those of the control group. On the other hand, the ASH group rather resembled the HCM group in the thickness and dynamics of the septal wall and the free wall as well as in the septal configuration. The most characteristic difference of the ASH and HCM groups from the SH group was in the significantly greater thickness of the septal wall at end diastole. However, in view of the developmental mechanism of hypertensive heart, it is interesting to note that the more the septal-free wall ratio increases, the more the thickness of the septal wall increases in the SH group.
