Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malondialdehyde (MDA) derivatives occur as normal constituents of rat and human urine. In a previous study, it was found that MDA excretion in rats is responsive to MDA intake and to certain factors that increase lipid peroxidation in vivo: vitamin E deficiency, iron administration and a high concentration of cod liver oil (CLO) fatty acids in the tissues. In the present study, the effect on MDA excretion of several additional dietary and endogenous factors was evaluated. The composition of dietary fatty acids had a major influence on MDA excretion in fed animals, being highest for animals fed n-3 fatty acids (20:5 and 22:6) from CLO, intermediate for those fed n-6 (18:2) acids from corn oil (CO) and lowest for those fed saturated acids from hydrogenated coconut oil (HCO). Diet was the main source of urinary MDA in all groups. Fasting produced a marked increase in urinary MDA, which tended to be higher in rats previously fed CLO. Fasting MDA excretion was not affected by the level of CO in the diet (5, 10 or 15%), indicating that feeding n-6 acids does not increase lipid peroxidation in vivo. Adrenocorticotropic hormone and epinephrine administration increased urinary MDA, further indicating that lipolysis either releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A decrease in fasting MDA excretion was observed in rats previously fed a high level of antioxidants (vitamin E + BHT + vitamin C) vs a normal level of vitamin E. MDA excretion increased following adriamycin and CCl4 administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo. 282 43

Retrolental fibroplasia is today the principal cause of blindness in children of preschool age, exceeding all other causes combined. The disease occurs in infants of low weight at birth, commonly those born prematurely. The incidence of the disease is rising at an alarming rate. Vitamin E deficiency, corticotropin (ACTH) deficiency, the use of cow's milk in place of mother's milk, and improper oxygenation have been suggested as etiologic factors but the cause remains a mystery. Often the incidence is high in institutions in which maximal care is given premature infants.Clinically, the disease advances through an "active" phase during which regression is possible, and a "subsiding" or "cicatricial" phase which terminates with the formation of a disorganized opaque mass behind the lens. The earliest manifestations are noted in the fundi. Hemorrhages, neovascularization, transudation commencing in the periphery, and retinal separation contribute to the formation of the characteristic retrolental membrane. The diagnosis may be made when the retrolental membrane is observed in the eye of an infant whose weight at birth was low. Differential diagnosis is required occasionally. Thus far, no form of therapy has prevented or reversed the pathologic changes successfully. Use of vitamin E, corticotropin and mother's milk has not influenced the incidence of the disease. Avoidance of premature delivery if possible is indicated.
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PMID:Retrolental fibroplasia; blindness in infants of low weight at birth. 1300 70

Excessive oxidative stress and associated macromolecular damage are considered to be key features of aging, and appear to contribute to the age-related decline in steroid hormone production in adrenal and testicular Leydig cells. The current studies were initiated to examine the potential mechanism by which excessive oxidative stress during aging attenuates the functional expression of the oxidant-responsive transcription factor Activator protein-1. Chronic oxidative stress was induced in vivo by maintaining groups of rats on a diet deficient in vitamin E for 6 months. Plasma, liver, and adrenal tissues from vitamin E-deficient animals had negligible levels of this vitamin and showed high susceptibility to in vitro lipid peroxidation. Synthesis and secretion of corticosterone in response to corticotropin (ACTH), dibutyryl-cAMP, or 20alpha-hydroxycholesterol in vitro was significantly reduced in adrenocortical cells prepared cells from rats deficient in vitamin E. AP-1 DNA-binding activity was diminished approximately 55 % in adrenal extracts from vitamin E-deficient rats with no corresponding change in the binding activity of SP-1. The vitamin E deficiency-mediated loss of AP-1 activity was not due to an alteration in the dimeric composition of constituent proteins, but rather to a general down-regulation of steady-state levels of members of the Fos and Jun families of proteins. Interestingly, vitamin E deficiency also reduced the expression of the redox-regulated Ref-1 protein. Collectively these data demonstrate that chronic oxidative stress specifically down-regulates essential components of the AP-1 transcription factor complex, and suggest that aberrancies in AP-1 expression may adversely affect processes crucial for intracellular cholesterol transport and steroid hormone production.
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PMID:Suppression of steroidogenesis and activator protein-1 transcription factor activity in rat adrenals by vitamin E deficiency-induced chronic oxidative stress. 1506 14