Respiration-coupled H+ ejection by mitochondria.
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Biomedical subjects
Publications and source records attributed to A Alexandre.
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In order to verify more directly our earlier measurements showing that, on the average, close to four vectorial H(+) are rejected per pair of electrons passing each of the three energy-conserving sites of the mitochondrial electron transport chain, direct tests of the H(+)/2e(-) ratio for sites 2 and 3 were carried out in the presence of permeant charge-compensating cations. Site 2 was examined by utilizing succinate as electron donor and ferricyanide as electron acceptor from mitochondrial cytochrome c; the directly measured H(+)/2e(-) ratio was close to 4. Energy-conserving site 3 was isolated for study with ferrocyanide or ascorbate plus tetramethylphenylenediamine as electron donors to cytochrome c and with oxygen as electron acceptor. The directly measured H(+)/2e(-) ratio for site 3 was close to 4. The H(+)/ATP ratio (number of vectorial H(+) ejected per ATP hydrolyzed) was determined with a new method in which the steady-state rates of both H(+) ejection and ATP hydrolysis were measured in the presence of K(+) + valinomycin. The H(+)/ATP ratio was found to approach 3.0. A proton cycle for oxidative phosphorylation is proposed, in which four electrochemical H(+) equivalents are ejected per pair of electrons passing each energy-conserving site; three of the H(+) equivalents pass inward to derive ATP synthesis from ADP and phosphate and the fourth H(+) is used to bring about the energy-requiring electrogenic expulsion of ATP(4-) in exchange for extramitochondrial ADP(3-), via the H(+)/H(2)PO(4) (-) symporter.
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A case of opsoclonus and palatal myoclonus following blunt head injury is described. The syndrome appeared 1 month after the injury and lasted unchanged until death. Postmortem examination showed the presence of widespread lesions of the brain stem affecting the dentato-rubro-olivary system. The main clinical features of the syndrome and their anatomical correlates are discussed.
A comprehensive study of the motor patterns, usually grouped under the heading "decerebrate rigidity," was carried out in a series of 800 patients with severe head injuries. The incidence of these manifestations was 39.6%, and when they were present chances of survival were reduced from 79.4% to 28.1%. Clinical and electromyographic investigations revealed heterogeneous and unstable motor manifestations that did not fit into the classical groups of experimental models of decerebrate rigidity. Combinations of extensor and flexor attitudes and/or responses were frequently found in same patient, but could be separated into homogeneous groups. Each recognized postural pattern had its own distinct neurological signs and prognosis. Age did not significantly affect the outcome, however, intracranial exapnding lesions (73.5%), impairment of the brain-stem oculomotor system (49.8%), and deep coma (88.9%) all contributed to an unfavorable course. Surgical treatment was effective when performed for intracranial hematomas and in patients with incomplete extensor rigidity. Good recovery was achieved in 16% of decerebrate patients, while 12.1% survived in prolonged coma or with severe disabilities. All clinical and neuropathological data suggest that extensor motor abnormalities in the acute phase of cerebral traumatic disease do not always conclusively indicate structural brain-stem damage. A critical analysis of so-called "decerebrate rigidity" (rejecting in some instances its Sherringtonian implications) may allow for a more accurate clinical assessment of the severity of head injury.
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