Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To prevent cataracts induced by glucocorticoids (GC) as a systemic disease, the suppression of oxidative stress caused by GC in the hepatic metabolism is of significant interest. In this study, to elucidate the formative mechanism of GC-induced cataracts, we examined the preventive effect and then analysed the mechanisms of thyroxine on GC-induced cataract formation. Fifteen day old chick embryos were administered with 0.25 micromol hydrocortisone succinate sodium (HC), and then 12-30 nmol of thyroxine 4 hr after HC administration. At the indicated time after HC treatment, we examined the incidence of cataract formation, the levels of serum glucose and lipids, lenticular and hepatic glutathione (GSH), and lipid peroxide (LPO) in the lens, blood and liver. Almost all lenses (96%) removed 48 hr after HC administration were opaque. Thyroxine prevented HC-induced cataract formation effectively, and suppressed the elevations of serum glucose and LPO in the lens, blood and liver. The treatment prevented the decreased lenticular GSH level at 48 hr, but the hepatic GSH level at 24 hr remained lowered in contrast to the results of previous studies using insulin. Moreover, thyroxine did not decrease the elevated serum lipid level (triglyceride and non-esterified fatty acid) caused by HC. Under thyroxine treatment, in constant to insulin, acceleration of GSH-GSSG cycle rather than GSH de novo synthesis keeps a certain level of hepatic GSH necessary for diminishing the elevation of LPO as a risk factor of GC-induced cataract formation. The regulation of metabolic changes ensured the maintenance of hepatic GSH level, which is necessary to reduce oxidative stress produced by GC and to protect the lens from oxidative stress leading to opacification.
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PMID:Suppressive effects of thyroxine on glucocorticoid (gc)-induced metabolic changes and cataract formation on developing chick embryos. 1138 52

Thyroxine-treated human lens epithelial cells, HLE B-3, were grown in either a normoxic or hyperoxic atmosphere as a first step in identifying factors related to their increased viability. Reactive oxygen species, ROS, and the apparent mitochondrial membrane potential, Delta Psi(m), were measured using fluorescent probes. ROS were significantly higher in HLE B-3 cells grown in a hyperoxic atmosphere for both thyroxine-treated and untreated samples. However, treatment with thyroxine produced 40% lower ROS levels than untreated cells. A mitochondrial uncoupler concomitantly reduced ROS generation. In cells that were grown in a hyperoxic atmosphere, the Delta Psi(m) was significantly higher for samples treated with thyroxine compared to those that were untreated. ROS generation correlated inversely with the apparent Delta Psi(m) and the amount of cardiolipin, and correlated with the amount of lipid oxidation products. These correlations were valid whether cardiolipin and the Delta Psi(m) were decreased as a result of oxygen or increased as a result of thyroxine treatment. Therapies that protect mitochondria from damage and reduce damaging ROS generation may potentially ameliorate the effects of oxidation that occur in aging tissues and in diseases such as cataract.
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PMID:Hyperoxia and thyroxine treatment and the relationships between reactive oxygen species generation, mitochondrial membrane potential, and cardiolipin in human lens epithelial cell cultures. 1860 Apr 90