Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036474 (scurvy)
685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mild and severe retinal photic injuries were inflicted on 22 eyes of seven monkeys fed a vitamin C-deficient diet and four monkeys given a vitamin C-enriched diet. The retinal lesions were studied by fundus examination, fluorescein angiography, and light and electron microscopy. While the general cellular response to photic injury in the retina of scorbutic animals was not different qualitatively from that in the normal animals, scurvy appeared to cause more severe tissue damage, an exaggerated repair response, and more advanced retinal degeneration. In the four groups of eyes, representing mild and severe photic injury in normal and scorbutic animals, a continuous spectrum of changes was produced. The least damage occurred from mild photic injury in the normal animals, and the most detrimental insult resulted from severe photic injury in the scorbutic animals. We propose that the basic mechanism by which ascorbate mitigates retinal photic injury depends on its redox properties. Ascorbate functions as an antioxidant in the retina. It scavenges superoxide radicals and hydroxyl radicals, quenches singlet oxygen, and reduces hydrogen peroxide, all of which are formed in retinal photic injury. This hypothesis provides an explanation for the high level of ascorbate in the retina. The pathogenetic mechanisms that correspond to the three distinct phases of pathologic changes observed in retinal photic injury are characterized. In phase 1, single oxygen is generated in a photodynamic reaction that damages the photoreceptor elements and pigment epithelium. In phase 2, macrophages attracted from the systemic circulation invade the subretinal space, and a photo-oxidative reaction generates superoxide radicals, hydrogen peroxide, and hydroxyl radicals. These free radicals attack the photoreceptor cells and pigment epithelium to cause further retinal damage. In phase 3, macrophages remain in the subretinal space for as long as 8 months after injury, causing persistent disruption of the blood-retinal barrier. The photo-oxidative reaction appears to linger, resulting in chronic retinal degeneration. It is hypothesized that in some forms of age-related macular degeneration, patients suffer from repeated mild photic insult throughout their lifetime. Aging has been associated with subclinical scurvy, which leads to even greater susceptibility to photic injury. Although ascorbate moderates many biochemical functions of the body and helps the retina ameliorate photo-oxidative injury, it should be regarded as a nutritional supplement to maintain health when consumed in appropriate amounts and not as a therapeutic agent for the treatment of severe insults.
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PMID:Retinal photic injury in normal and scorbutic monkeys. 344 41

The objectives of this study were to determine ascorbic acid stability and its effect on antiproteinase activity of seminal plasma in the presence of an oxidant. Effect of seminal plasma, and additives: glutathione, albumin, hydrogen peroxide and Tris buffer, on ascorbic acid degradation was investigated by UV absorbance. Antiproteinase against trypsin amidase activity was measured spectrophotometrically using N-benzoyl-DL-arginine-p-nitroanilide (BAPNA) as substrate. Ascorbic acid was destroyed much more rapidly with the addition of hydrogen peroxide than in Tris buffer at pH 8.2 alone. Seminal plasma protected ascorbic acid more efficiently than glutathione and albumin alone. The protective effect of seminal plasma on ascorbic acid degradation may closely relate to the function of ascorbic acid in reproductive system of scurvy-prone animals including teleost fish. Within the range of 1-8 mM concentrations, ascorbic acid had a pro-oxidant action on seminal plasma antiproteinase activity in vitro when they were incubated with hydrogen peroxide.
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PMID:Protective effect of seminal plasma proteins on the degradation of ascorbic acid. 747 34

Foods generally contain special ingredients which easily to interact with drugs human intaking, thus affecting drug efficacy and excretion, and even cause adverse reactions. Vitamin C (Vit. C) is abundant in fresh fruits and vegetables. It plays a regulatory role in redox metabolism, and its absence can cause scurvy. Aspirin (ASP) can be used to treat many diseases, is the earliest, common and widely used as antipyretic, analgesic and antirheumatic medicine. Human serum albumin (HSA) is the most abundant protein in vertebrate plasma and has the property of combining and transporting endogenous and exogenous substances. In this paper, the effects of Vit. C on the combination of ASP and HSA were studied by multi-spectra and voltammetric approaches. Fluorescence spectra showed that the quenching mode between Vit. C and HSA is dynamic, and the main binding force is hydrophobic force. The quenching mode between ASP and HSA is static one, and the main binding force is hydrogen bond and van der Waals force. For ternary biological system of (HSA-ASP)-Vit. C, the binding constant decreases compared with HSA-Vit. C system. However, for (HSA-Vit. C)-ASP system, the binding constant does not change when compared with binary system of HSA-ASP. Based on the technology combination of voltammetry, infrared, three-dimensional fluorescence and circular dichroism (CD), it is proved that the existence of ASP will influence the binding process of Vit. C to HSA. It could be concluded that taking Vit. C first doesn't affect the absorption of ASP and may be good for health; in contrast, it is not good to take Vit. C immediately as one have just taken ASP, because the existence of ASP reduce the absorption of Vit. C for human body.
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PMID:Interaction between aspirin and vitamin C with human serum albumin as binary and ternary systems. 3232 8