succinate dehydrogenase/atrofia

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Partial inhibition of brain succinate dehydrogenase by 3-nitropropionic acid is sufficient to initiate striatal degeneration in rat.

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Chronic inhibition of succinate dehydrogenase (SDH) by systemic injection of the selective inhibitor 3-nitropropionic acid (3NP) has been used as an animal model for Huntington's disease (HD). However, the mechanisms by which 3NP produces lesions in the striatum are not fully characterized. A

Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 4. Changes in the activity of succinate dehydrogenase and the levels of transferrin and ferritin in the Sertoli and germ cells.

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A single oral dose of di-n-butyl phthalate (DBP) to male rats caused a sloughing of the germ cells at 6 h both with a decrease in the activity of succinate dehydrogenase (SDH) in the Sertoli cells and in the Sertoli-germ connection and with an increase in the activity of lactate dehydrogenase (LDH)

[Optic atrophy and ataxia (complex II deficiency-mutation in Fp subunit gene of succinate dehydrogenase)].

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Autophagy-associated atrophy and metabolic remodeling of the mouse diaphragm after short-term intermittent hypoxia.

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BACKGROUND Short-term intermittent hypoxia (IH) is common in patients with acute respiratory disorders. Although prolonged exposure to hypoxia induces atrophy and increased fatigability of skeletal muscle, the response to short-term IH is less well known. We hypothesized that the diaphragm and limb

The SDH mutation database: an online resource for succinate dehydrogenase sequence variants involved in pheochromocytoma, paraganglioma and mitochondrial complex II deficiency.

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BACKGROUND The SDHA, SDHB, SDHC and SDHD genes encode the subunits of succinate dehydrogenase (succinate: ubiquinone oxidoreductase), a component of both the Krebs cycle and the mitochondrial respiratory chain. SDHA, a flavoprotein and SDHB, an iron-sulfur protein together constitute the catalytic

[Histochemical study on disuse atrophy of skeletal muscle in rabbit (author's transl)].

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Histological and histochemical study was carried out to investigate disuse atrophy on skeletal muscle in adult albino rabbits. Untreated anterior tibial muscle and gastrocnemius muscle were studied. Three fiber types were recognized with myosin ATPase reaction, viz. type I, IIA and IIB fibers under

Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 2. The effects on some testicular enzymes.

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A single oral dose of di-n-butyl phthalate (DBP) to male rats caused histologically a sloughing of the germ cells at 6 h. On Days 1 and 2 more severe sloughing was seen, followed by atrophy and the dissociation of the germ cells from the Sertoli cells and the spermatogonia. Biochemically, there was

Effect of adriamycin on the activity of the succinate dehydrogenase-coenzyme Q10 reductase of the rabbit myocardium.

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Rabbits were injected with adriamycin 3 days/week/7 weeks. Heart tissues of treated rabbits showed myocardial degeneration, but the tissues of controls were normal. The deficiency in the activity of the succinate dehydrogenase-coenzyme Q10 reductase in the heart tissues of the rabbits treated with

Central core degeneration after tenotomy in soleus muscles of hyperthyroid rats.

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Tenotomy of the rat soleus muscle is followed by a central degeneration of slow, fatigue-resistant muscle fibers. Previous experiments showed that fast, fatigable fibers of the gastrocnemius when transformed to slow, fatigue-resistant fibers by cross-reinnervation also develop lesions after

Age-related macular degeneration. The lipofusion component N-retinyl-N-retinylidene ethanolamine detaches proapoptotic proteins from mitochondria and induces apoptosis in mammalian retinal pigment epithelial cells.

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10-20% of individuals over the age of 65 suffer from age-related macular degeneration (AMD), the leading cause of severe visual impairment in humans living in developed countries. The pathogenesis of this complex disease is poorly understood, and no efficient therapy or prevention exists to date. A

Succinate Dehydrogenase B (SDHB) Immunohistochemistry for the Evaluation of Muscle Biopsies.

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Succinate dehydrogenase (SDH) is a key mitochondrial enzyme complex composed of 4 subunits. SDH histochemistry is routinely utilized in the assessment of muscle biopsies to reveal underlying pathology such as subsarcolemmal mitochondrial aggregates. In this study, we evaluated the utility of

[Succinate dehydrogenase activity in the mesonephros in the process of development of chick embryos].

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The activity of succinate dehydrogenase in the mesonephros tissue of chick embryos is rather high on the 6th day of embryonal development and is not subjected to significant changes up to the 17th day. The absence of wide variations in the activity of this enzyme during the period of degeneration of

Succinate dehydrogenase and mitochondria in the hair cells in the organ of Corti of mature and old shaker-1 mice.

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The activity of succinate dehydrogenase in the sensory hair cells in the organ of Corti of mature and old shaker-1 mice described as the animals grew older, the outer hair cells being the most effected. The decrease inactivity of this enzyme was closely linked with the degeneration of the

The differential JunB responses to inhibition of succinate dehydrogenase in rat hippocampus and liver.

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The inhibitor of mitochondrial enzyme succinate dehydrogenase, 3-nitropropionic acid (3-NPA), induces cellular energy deficit followed by oxidative stress, secondary excitotoxicity and neuronal degeneration. The fast activation of Jun and Fos proteins and other proteins encoding inducible

FEATURES OF HISTOCHEMICAL CHANGES IN THE ACTIVITY OF SUCCINATE DEHYDROGENASE OF ARTIFICIAL BLADDER IN DYNAMICS (EXPERIMENTAL STUDY).

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The gold standard for the treatment of invasive bladder cancer recognized throughout the world is radical cystectomy with orthotopic ileocystoplasty using the ileal intestinal tract. The study of the effect of urine on the adaptation of the mucosa of the artificial bladder continues for the last

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