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Higher succinate than acetate levels differentiate cerebral degenerating cysticerci from anaerobic abscesses on in-vivo proton MR spectroscopy.
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We present three patients with large intraparenchymal isolated degenerating cysticerci in whom the diagnosis was primarily based on in-vivo proton MR spectroscopy, and subsequently confirmed histologically. We suggest that the presence of succinate alone or more succinate acetate indicates the
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)
Protective effects of vitamin A and vitamin E succinate against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced body wasting, hepatomegaly, thymic atrophy, production of reactive oxygen species and DNA damage in C57BL/6J mice.
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The protective effect of vitamin A and vitamin E succinate against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced acute toxicity and measures of oxidative stress was studied. Ten mice were treated with either vitamin A (50 mg/kg every other day for eight days) or vitamin E succiante (150
[Optic atrophy and ataxia (complex II deficiency-mutation in Fp subunit gene of succinate dehydrogenase)].
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Application and interpretation of genome-wide association (GWA) studies for informing pharmacogenomic research - examples from the field of age-related macular degeneration.
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Genome-wide association (GWA) studies apply broad DNA scans on hundreds-of-thousands of common sequence variants in thousands of people for the purpose of mapping trait- or disease-related loci. We provide examples of ligand- and target-based studies from the field of age-related macular
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
Antioxidant effects of pH-regulating agents on the thermal deterioration of vegetable oils.
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pH-Regulating agents, such as sodium tartrate, disodium succinate, and trisodium citrate, were investigated for their antioxidant activities during the thermal deterioration of vegetable oils. Refined rapeseed and rice bran oils, supplemented with pH-regulating agents and α-tocopherol (0.1%) were
[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
Pharmacologic rescue of lethal seizures in mice deficient in succinate semialdehyde dehydrogenase.
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Succinate semialdehyde dehydrogenase (ALDH5A1, encoding SSADH deficiency is a defect of 4-aminobutyric acid (GABA) degradation that manifests in humans as 4-hydroxybutyric (gamma-hydroxybutyric, GHB) aciduria. It is characterized by a non-specific neurological disorder including psychomotor
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
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