tretinoin and Optic-Atrophy--Hereditary--Leber

tretinoin has been researched along with Optic-Atrophy--Hereditary--Leber* in 1 studies

Other Studies

1 other study(ies) available for tretinoin and Optic-Atrophy--Hereditary--Leber

Article	Year
Glutathione depletion in antioxidant defense of differentiated NT2-LHON cybrids. Neurobiology of disease, 2007, Volume: 25, Issue:3 The mechanism of retinal ganglion cell loss in Leber's hereditary optic neuropathy (LHON) is still uncertain, and a role of enhanced superoxide production by the mutant mitochondrial complex I has been hypothesized. In the present study, it was shown that LHON cybrids, carrying the np11778 mutation, became selectively more H(2)O(2) sensitive compared with the parental cell line only following short-term retinoic acid differentiation. They contained a decreased cellular glutathione pool (49%, p< or =0.05), despite 1.5-fold enhanced expression of the regulatory subunit of gamma-glutamylcysteine synthetase (p< or =0.05). This points to a reduction of the capacity to detoxify H(2)O(2) and to changes in thiol redox potential. The activity of the H(2)O(2) degrading enzyme glutathione peroxidase (GPx) and the activities of glutathione reductase (GR) and superoxide dismutase (SOD) were unaffected. Topics: Antineoplastic Agents; Antioxidants; Cell Differentiation; Cell Line, Tumor; Electron Transport Complex I; Genotype; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Humans; Hydrogen Peroxide; Mitochondria; Optic Atrophy, Hereditary, Leber; Oxidants; Point Mutation; Superoxide Dismutase; Teratoma; Tretinoin	2007

Article

Year

Glutathione depletion in antioxidant defense of differentiated NT2-LHON cybrids.

Neurobiology of disease, 2007, Volume: 25, Issue:3

The mechanism of retinal ganglion cell loss in Leber's hereditary optic neuropathy (LHON) is still uncertain, and a role of enhanced superoxide production by the mutant mitochondrial complex I has been hypothesized. In the present study, it was shown that LHON cybrids, carrying the np11778 mutation, became selectively more H(2)O(2) sensitive compared with the parental cell line only following short-term retinoic acid differentiation. They contained a decreased cellular glutathione pool (49%, p< or =0.05), despite 1.5-fold enhanced expression of the regulatory subunit of gamma-glutamylcysteine synthetase (p< or =0.05). This points to a reduction of the capacity to detoxify H(2)O(2) and to changes in thiol redox potential. The activity of the H(2)O(2) degrading enzyme glutathione peroxidase (GPx) and the activities of glutathione reductase (GR) and superoxide dismutase (SOD) were unaffected.

Topics: Antineoplastic Agents; Antioxidants; Cell Differentiation; Cell Line, Tumor; Electron Transport Complex I; Genotype; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Humans; Hydrogen Peroxide; Mitochondria; Optic Atrophy, Hereditary, Leber; Oxidants; Point Mutation; Superoxide Dismutase; Teratoma; Tretinoin

2007