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PubMed1983

[Protein synthesis and oxidative activity of the brain in oxygen deficiency].

Biochemical and electron microscopic research methods showed disorders of the metabolism and the ultrastructure of the rat brain under the impact of experimental hypoxia and anoxia. Two to 3.5 hours after the exposure, the synthesis of protein in the neuronal fractions was impaired and the activity of the oxidative enzymes in the subfractions of synaptosomes and mitochondria was inhibited. The tissue ultrastructure was also impaired which was most pronounced in the synaptic processes of neurones. The data indicate fine morphochemical correlations at the subcellular level in the period immediately following post-hypoxic brain survival.

Adenosine Triphosphatases↗
PubMed1983

Identification of nonmitochondrial creatine kinase enzymatic activity in isolated sea urchin mitotic apparatus.

ATP-dependent calcium sequestration was previously localized in vesicles of mitotic apparatus isolated from sea urchins. We now demonstrate that the mitotic apparatus contains an ATP-regenerative system characterized as creatine kinase (EC 2.7.3.2). Mitotic apparatus isolated with vesicles intact converted ADP to ATP if phosphocreatine was present. Omission of ADP or phosphocreatine gave negligible ATP. When mitotic apparatus were washed with detergent-containing buffer to remove vesicles, their ability to produce ATP from ADP and phosphocreatine was reduced. Assays of creatine kinase activity using NADP+:glucose-6-phosphate dehydrogenase indicated that 70% of the creatine kinase activity was extractable with 0.5% Triton X-100. The insoluble residue containing the skeleton of the mitotic apparatus had the rest of the activity. Experiments with a luciferin/luciferase assay showed that Triton removed above 82% of the activity. Preparations of intact mitotic apparatus were free of cytochrome c oxidase (EC 1.9.3.1) activity and therefore free of mitochondria. About 10(8) mitotic apparatus (total volume about 1 liter) could produce 17 mmol of ATP/min when substrates were not limiting. The creatine kinase enzyme activity described herein and the previously described membrane vesicular calcium sequestration system are nonmitochondrial, integral constituents of the sea urchin mitotic apparatus.

Creatine Kinase↗
PubMed1994

Cytochrome c oxidase activity in osteoclasts appeared in an early stage of parathyroid hormone treatment.

Osteoclasts which appeared in an early stage of parathyroid hormone (PTH) administration were examined using cytochrome c oxidase activity. In the period of 1-2 hr after intraperitoneal administration of PTH, two types of osteoclasts were observed. The first type had a well-developed ruffled border characterized by deeply infolded extracellular channels, and many endocytic vacuoles were observed, as seen in control osteoclasts. Many of the mitochondria contained in the first type were with the reaction products of the enzyme on the crystal membrane and within the intermembrane space (type 1 mitochondria), and the distribution of type 1 mitochondria was similar to that seen in control osteoclasts. The second type had a ruffled border characterized by unclear extracellular channels and cytoplasmic projections. The numerical percentage of type 1 mitochondria in the second type of osteoclasts (45.3%) was significantly smaller than that in the first type (79.9%). Mitochondria which had the reaction products of the enzyme only on the crystal membrane including those with no reaction product (type 2 mitochondria) were predominant in the second type of osteoclasts. These results include two possible ways in which a morphologically regressive change of the ruffled border can occur in osteoclasts during an early stage of PTH treatment, and cytochrome c oxidase activity is closely associated with the change in the ruffled border.

Animals↗
PubMed1998

Dedifferentiated cardiomyocytes from chronic hibernating myocardium are ischemia-tolerant.

Left ventricular biopsies from 21 patients with clinically diagnosed chronic hibernating myocardium (CHM) were examined by light- and electron microscopy. A mean of 27% of cardiomyocytes were structurally altered and were characterized as hibernating, because of reduced amount of myofibrils and increased glycogen content. Electron microscopy of these cells showed reduction of T-tubules and numerous small mitochondria, but few changes associated with degeneration, acute ischemia or apoptosis. The structural changes found in CHM are reminiscent of dedifferentiation rather than degeneration. The expression patterns of some structural proteins show resemblance with those in embryonic cardiomyocytes. Histochemically, mitochondrial NADH-oxidase and proton translocating ATPase activities were absent, whereas cytochrome c activity was present. Intracellular calcium distribution indicated normally bound sarcolemmal calcium and absence of excess mitochondrial calcium accumulation. Nuclear chromatin ranged from normal to dispersed with only a few nuclei that were clumped. These results suggest that cardiomyocytes from human CHM hearts are structurally altered, but viable, and lack morphologic and cytochemical characteristics suggestive of apoptosis or acute ischemia.

Apoptosis↗
PubMed1986

The localization of cytochrome oxidase in the LGN and striate cortex of postnatal kittens.

The distribution of cytochrome oxidase (C.O.) was examined in the lateral geniculate nucleus of the kitten during the first postnatal month and compared with the adult pattern. During the first week, most of the C.O. was localized within the perikarya of geniculate neurons. Perigeniculate neurons had darkly reactive dendrites as well as perikaya. A population of relatively large, darkly reactive neurons became distinguishable around the end of the first week, as the level of reactivity diminished to moderate-to-light within most medium and small neurons. On the basis of their relative size and pattern of distribution, most of the darkly reactive neurons are likely to represent ones that will later have class 1 morphology and develop Y receptive field properties. These cells normally undergo rapid growth earlier, and their growth is more adversely affected by early short-term monocular suture than other classes of less reactive geniculate neurons. Thus, in the LGN of developing kitten, C.O. histochemistry may be used as a functional marker for future class 1 Y-cells. The reactivity of the neuropil gradually increases as synapses with dendrites mature. At the electronmicroscopic level the increased reactivity of the neuropil is due mainly to an increase in the number of reactive mitochondria localized within the growing dendrites. In the developing striate cortex of postnatal kittens dark reactivity is localized in the outer part of layer II for the first 2 weeks and then disappears. Dark reactivity gradually increases in layer IV after the third week. The changes in C.O. reactivity accompany pathway-specific physiological and anatomical changes that occur during early postnatal development.

Animals↗
PubMed1996

Morphological-cytochemical and molecular genetic analyses of mitochondria in isolated human oocytes in the reproductive age.

Molecular genetic, cytochemical and morphometric analyses have been performed on isolated oocytes from 41 women (27-39 years of age) in order to detect mutations of mitochondrial DNA (mtDNA), defects of the respiratory chain (ubiquinone-cytochrome-c-oxidoreductase = complex III; cytochrome-c-oxidase = complex IV) and alterations of mitochondrial volume during cellular ageing. Morphometric analyses showed an increase in mitochondrial numerical density with age from the mean values of 7.36 per micron2 and 6.97 per micron3 up to 30 years to 10.74 per micron2 and 11.66 per micron3 in the age group 31-40 years (P < 0.001). Similarly, an increase in the mitochondrial profile area from 0.074 per micron2 in the age group < 30 years to 0.101 per micron2 was noted in the fourth decade. The mitochondrial volume fraction was also significantly increased in the elder age group. Neither point mutations of mtDNA (nucleotide pairs 3243, 8344) nor the common deletion (4977 bp, nucleotide pairs 8482-13460) could be detected. In parallel, ultra- and immunocytochemical studies of the complexes III-IV failed to reveal functional defects. In conclusion there is an age-related increase in the volume fraction of the mitochondria which might reflect subtle changes in the oxidative phosphorylation capacity, but is not linked to mutations of mtDNA or functional defects of the respiratory chain enzymes in mature human oocytes from women of reproductive age.

Adult↗
PubMed2004

Inactivation of mitochondrial electron transport by photosensitization of a pheophorbide a derivative.

We examined the damage to mitochondrial electron transport caused by photosensitization of a pheophorbide a derivative, DH-I-180-3, shown recently to induce necrosis of lung carcinoma cells with low dark toxicity. Confocal microscopy showed that DH-I-180-3 co-localized with dihydrorhodamine-123 suggesting that it mainly accumulates in mitochondria. The photosensitizer alone in the dark did not affect mitochondrial electron transport. Illumination of isolated mitochondria in the presence of DH-I-180-3 resulted in inhibition of both NADH- and succinate-dependent respiration. Measurement of the activity of each component of the electron transport chain revealed that Complex I and III were very susceptible to the treatment whereas Complex IV was resistant. We conclude that the photosensitizer is localized in mitochondria and, upon illumination, produces reactive oxygen species that inactivate Complexes I and III.

Animals↗
PubMed2000

Ascorbate biosynthesis in mitochondria is linked to the electron transport chain between complexes III and IV.

Ascorbic acid is synthesized from galactono-gamma-lactone (GL) in plant tissues. An improved extraction procedure involving ammonium sulfate precipitation of membrane proteins from crude leaf homogenates yielded a simple, quick method for determining tissue activities of galactono-gamma-lactone dehydrogenase (GLDH). Total foliar ascorbate and GLDH activity decreased with leaf age. Subcellular fractionation experiments using marker enzymes demonstrated that 80% of the total GLDH activity was located on the inner mitochondrial membrane, and 20% in the microsomal fraction. Specific antibody raised against potato (Solanum tuberosum L.) tuber GLDH recognized a 56-kD polypeptide in extracts from the mitochondrial membranes but failed to detect the equivalent polypeptide in microsomes. We demonstrate that isolated intact mitochondria synthesize ascorbate in the presence of GL. GL stimulated mitochondrial electron transport rates. The respiration inhibitor antimycin A stimulated ascorbate biosynthesis, while cyanide inhibited both respiration and ascorbate production. GL-dependent oxygen uptake was observed in isolated intact mitochondria. This evidence suggests that GLDH delivers electrons to the mitochondrial electron transport chain between complexes III and IV.

Amino Acid Sequence↗
PubMed1996

Metabolic and neurochemical plasticity of gamma-aminobutyric acid-immunoreactive neurons in the adult macaque striate cortex following monocular impulse blockade: quantitative electron microscopic analysis.

The purpose of the present study was to examine the effects of retinal impulse blockade on gamma-aminobutyric acid (GABA)-immunoreactive (GABA-IR) neurons in cytochrome oxidase (CO)-rich puffs of the adult monkey striate cortex. Specifically, we wished to know if changes occurred in their CO activity, GABA immunoreactivity, and synaptic organization. A double-labeling technique, which combined CO histochemistry and postembedding GABA immunocytochemistry on the same ultrathin sections, was used to reveal simultaneously the distribution of the two markers. We quantitatively compared changes in GABA-IR neurons of deprived puffs (DPs) with respect to non-deprived puffs (NPs) 2 weeks after monocular tetrodotoxin treatment. We found that the proportion of darkly CO reactive mitochondria in GABA-IR neurons of DPs drastically decreased to about half of those in NPs. There was a greater reduction of CO levels in GABA-IR axon terminals than in their cell bodies and dendrites. In contrast, most non-GABA-IR neurons displayed no significant change in their CO levels. Morphologically, GABA-IR neurons and axon terminals in DPs showed a significant shrinkage in their mean size. GABA immunoreactivity, as indicated by the density of immunogold particles in GABA-IR neurons, declined in DPs, and a greater decrease was also found in axon terminals than in cell bodies or dendrites. Moreover, the numerical density of GABA-IR axon terminals and synapses in DPs was significantly reduced without changes in that of asymmetric and symmetric synapses. Thus, the present results support the following conclusions: 1) Oxidative metabolism and neurotransmitter expression in GABA-IR neurons are tightly regulated by neuronal activity in adult monkey striate cortex; 2) GABA-IR neurons are much more vulnerable to functional deprivation than non-GABA-IR ones, suggesting that these inhibitory neurons have stringent requirement for sustained excitatory input to maintain their heightened oxidative capacity; and 3) intracortical inhibition mediated by GABA transmission following afferent deprivation may be decreased in deprived puffs, because the oxidative capacity and transmitter level in GABAergic neurons, especially in their axon terminals, are dramatically reduced.

Animals↗
PubMed1998

Immunocytochemical localization of substance P receptor in rat periaqueductal gray matter: a light and electron microscopic study.

The distribution of substance P receptor (SPR) protein in the rat periaqueductal gray matter (PAG) was investigated with a polyclonal antibody in the four subdivisions obtained by cytochrome-oxidase histochemistry (Co-hi). At light microscopic analysis, immunoreactivity appeared particularly dense in the dorsal subdivision of the PAG, was less intense in the other subdivisions, and formed several longitudinally organized columns. SPR-like immunoreactivity (SP(R-i)) was localized mostly to cell bodies and dendrites of small and medium-sized neurons, which constituted about 6% of the total neuronal population of the PAG. At the electron microscopic level, SP(R-i) could be observed on postsynaptic as well as on nonsynaptic regions of both cell bodies and dendrites. A small proportion of axons (4.2%) and axon terminals (5.3%) showed SP(R-i), the majority of labeled axon terminals, amounting to about 70% of synapsing elements, formed asymmetric synapses with dendrites. Rare astroglial processes displaying SP(R-i) were also observed scattered throughout the neuropil of all PAG subdivisions. Our observations suggest that 1) also in the PAG, SP may act in a diffuse, nonsynaptic manner, probably on targets that are distant from its sites of release; and 2) SP may modulate excitatory neurotransmission acting presynaptically on those labeled axons that form asymmetric synapses.

Animals↗