Assembly of cytochrome c. Apocytochrome c is bound to specific sites on mitochondria before its conversion to holocytochrome c.
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Apoenzymes↗
Biomedical subjects
B Hennig
Publications and source records attributed to B Hennig.
Change of cytochrome c structure during development of the mouse.
The structure of cytochrome c during mouse development is investigated. For this purpose the amino acid sequence of cytochrome c of the adult mouse had to be determined. The structure of cytochrome c of adult differentiated mouse cells differs in two amino acid residues from the known amino acid sequence of rabbit cytochrome c. No indication of different forms of cytochrome c in the adult differentiated cells was obtained. The structure of cytochrome c from 11.5-day-old mouse embryos is identical with that of adult mouse tissues. Since germ cells after meiotic division are the immediate precursors of a new individual, the structure of cytochrome c from sperm-containing mice testes was investigated. By means of chromatography of the cytochrome c and of peptide maps and amino acid analyses of its tryptic peptides, it is shown that mouse testis contains two isocytochromes c in about equal amount. The structure of one of these two isocytochromes c is identical with the structure of the adult-type cytochrome c of mouse. The testis-specific cytochrome c, which is assumed to be located in the sperm cells, differs in 13 of its 104 amino acid residues from the adult-type cytochrome c. From comparison of the primary and the spatial structures of the adult-type and the sperm-type isocytochromes c with the known structures of cytochrome c of more than 65 different species it is concluded that the duplication of the cytochrome c structural gene, causing the existence of the two ontogenetic-specific isocytochromes c in mouse, has occurred early in the evolution of eucaryotes.
Aging↗
Stent implantation for recurrent interatrial obstruction in an infant with hypoplastic left heart syndrome.
We report the case of a 19-month-old girl with hypoplastic left heart syndrome who, after Norwood stage 1 and 2 procedures, developed recurrent interatrial obstruction and was treated effectively with stent implantation. The stent was explanted electively 14 months after implantation and showed almost no endothelium formation. Therefore, there was no need for redo atrioseptectomy and the surgical intervention could be staged electively.
Blood Vessel Prosthesis Implantation↗
[Idiopathic left ventricular tachycardia in childhood: typical clinical findings and different therapeutic options].
We report 3 adolescents with structurally normal heart who were referred to hospital due to long-lasting palpitations. Initial 12-lead-ECG showed sustained, monomorphic ventricular tachycardia, right bundle branch block QRS morphology and axis deviation. After failure of different anti-arrhythmic drugs finally the intravenous medication with verapamil led to termination of ventricular tachycardia in all three patients. All clinical findings and the responsiveness to verapamil are consistent with the diagnosis of idiopathic left ventricular tachycardia. In one patient an electrophysiological study was done and increased left ventricular vulnerability was shown. After inducing a tachycardia originating from the left ventricle radiofrequency catheter ablation of the left-posterior fascicle was successfully performed. The tachycardia was not inducible after this ablation. Since that investigation the patient has been asymptomatic without anti-arrhythmic treatment. Two of three patients have been on oral verapamil prophylactically and have been free of symptoms.
Administration, Oral↗
Exposure to free fatty acid increases the transfer of albumin across cultured endothelial monolayers.
An initial exposure to high concentrations of free fatty acid increased the transfer of albumin across cultured endothelial monolayers. The rate and amount of albumin transfer was dependent on the oleic acid concentration to which the cultures were initially exposed, with 300 microM producing the maximum transfer. The albumin transfer also increased with the increasing time of exposure to oleic acid, the maximum effect occurring during the first 24 hours. An exposure to 300 microM linoleic acid produced an even greater increase in albumin transfer than did 300 microM oleic acid. The increased albumin transfer observed when cells were exposed to high concentrations of free fatty acid was largely reversible after reincubation of the cell monolayers in free fatty acid-poor media. In parallel experiments, radioactive oleic acid incorporation into cell triglycerides increased linearly as the fatty acid concentration was raised, with cell triglyceride content increasing up to sevenfold after incubation in a medium containing 300 microM oleic acid. A significant amount of oleic acid was incorporated into phospholipids, and the fatty acid composition of the endothelial triglycerides and phospholipids was modified. All these effects of oleic occurred without altering the incorporation of leucine into the cell protein. These results indicate that exposure to high concentrations of free fatty acid can alter endothelial cell lipid composition, and that this increases the albumin transfer across endothelium. This process might permit more macromolecules to enter the arterial wall.
Albumins↗
Zinc and endothelial function.
Zinc (Zn), an essential trace element, has antioxidant functions, stabilizes membranes, and plays a role in the activity of a host of Zn metalloenzymes. Zn deficiency has been shown to increase erythrocyte fragility, decrease the Zn content of the erythrocyte membrane, and alter erythrocyte membrane fluidity. Recent studies have shown that Zn deficiency induced by various mechanisms disrupts endothelial barrier cell function in vitro, and this was corrected with Zn supplementation. Moreover, physiological amounts of Zn attenuated the barrier dysfunction produced by the inflammatory cytokine tumor necrosis factor. These data have important implications for acute vascular processes, e.g., adult respiratory distress syndrome, and chronic vascular processes, e.g., atherosclerosis. The mechanisms by which Zn may affect endothelial cell function and attenuate cytokine-induced endothelial cell dysfunction are important areas of continuing investigation.
Arteriosclerosis↗
Nutrition and endothelial cell integrity: implications in atherosclerosis.
Loss of functional integrity of the vascular endothelium may be one of the initiating events in the etiology of atherosclerosis. Endothelial cells interact with blood components and the abluminal tissues, thus playing an active role in many aspects of vascular functions, such as permeability and vessel tone regulation. Endothelial cells constantly are exposed to nutrients which can modulate enzymes, receptors, transport molecules and various vasoactive mediators, resulting in significant functional changes of the endothelium and the underlying tissues. Nutrition may play an important role in the atherosclerotic disease process. There is evidence that certain vitamins and minerals prevent some metabolic and physiological perturbations of the vascular endothelium. This review focuses on selected lipids which cause endothelial cell injury or dysfunction and on nutrients which may exhibit antiatherogenic properties by being able to function as antioxidants or membrane stabilizers.
Animals↗
Antiestrogens inhibit endothelial cell growth stimulated by angiogenic growth factors.
We have previously reported that the partial estrogen antagonists, tamoxifen, clomiphene and nafoxidine, inhibited angiogenesis in vivo in a dose-related manner in the six-day old chick egg chorioallantoic membrane (CAM) assay. In the present study, we investigated the effect of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) on the growth of porcine pulmonary artery and human dermal microvascular endothelial cells. Both of these growth factors significantly increased the growth of these cells. The antiproliferative activity of the partial antiestrogens, tamoxifen, nafoxidine and clomiphene, and the pure antiestrogen, ICI 182,780, was determined. Tamoxifen, clomiphene, nafoxidine and ICI 182,780 significantly inhibited endothelial cell growth stimulated by bFGF and VEGF. This inhibition of endothelial cells was not altered by the presence of up to 30 microM of estradiol-17 beta. These results indicate that the antiangiogenic action of the antiestrogens does not occur via the estrogen receptor, but by a direct inhibition of growth factor stimulated endothelial cell growth.
Animals↗