Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT03226 (vitamin E)
 17,558 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Albino hairless mice (Skh:HR-1) exposed chronically to suberythemal doses of ultraviolet radiation develop visible skin changes, histological alterations, and tumors. Topical treatment of mice with solutions of superoxide-scavenging antioxidants (such as alpha-tocopherol, ascorbic acid, propyl gallate and Trolox) prior to each UVB radiation exposure reduced significantly the severity of these events. Tocopherol esters and ascorbyl palmitate were not as effective as the parent compounds in providing protection. The data suggest a role for superoxide in UVB radiation-induced skin photoaging and the protective potential of superoxide scavengers. In contrast, the severity of UVA radiation-induced mouse skin damage was not reduced by topical application of the antioxidants tested here.
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PMID:Photoprotective effect of superoxide-scavenging antioxidants against ultraviolet radiation-induced chronic skin damage in the hairless mouse. 216 96

Essential fatty acid deficiency was documented in a 3-year-old boy with chronic cholestasis secondary to paucity of intrahepatic bile ducts (Alagille's syndrome). Dietary management had consisted almost exclusively of a proprietary formula with over 80% of the fat as medium-chain triglycerides. The bullous lesions involved mostly sun-exposed areas and were diagnosed initially as being compatible with acquired porphyria cutanea tarda. Improvement followed correction of the fatty acid abnormalities with a polyunsaturated fat supplement administered orally. We postulate that the association of fatty acid deficiency and abnormal vitamin E status contributed to skin damage, possibly involving photosensitizing compounds poorly cleared by the markedly cholestatic liver.
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PMID:Essential fatty acid deficiency mimicking porphyria cutanea tarda in a patient with chronic cholestasis. 230 77

This study investigates whether supplementation with topical RRR-alpha-tocopherol (Eol), topical RRR-alpha-tocopheryl succinate, and oral RRR-alpha-tocopheryl acetate can reduce the incidence of acute and chronic damage to the skin (i.e., sunburn and pigmentation and skin cancer, respectively) induced by ultraviolet (UV) irradiation to mice. Groups of twenty Skh:2 female hairless pigmented mice were treated with 1) lotion vehicle, 2) 5% Eol lotion, 3) 5% topical RRR-alpha-tocopheryl succinate lotion, or 4) lotion vehicle and oral RRR-alpha-tocopheryl acetate. Within each group, 15 mice were exposed to 0.24 J/cm2 of UV-B radiation three times per week. The animals' weights and food intakes were monitored, and the vitamin E concentrations of skin, liver, and adipose tissue were measured to determine whether the topical Eol resulted in significant tissue levels. Skin pigmentation was scored, and the total number of clinically detectable skin tumors per animal was counted weekly. Results showed that the skin concentrations of Eol, as well as levels in the adipose tissue, were increased after topical application. Mice treated with each form of vitamin E showed no signs of toxicity and had significantly less acute and chronic skin damage induced by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer.
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PMID:Effects of topical and oral vitamin E on pigmentation and skin cancer induced by ultraviolet irradiation in Skh:2 hairless mice. 1134 Oct 50

Skin plays an important role in protection against oxidative stressors such as ultraviolet radiation, ozone and chemicals. Chronic sun exposure causes degenerative changes in the skin that are recognized as photoaging. Oxidative stress has been shown to alter the expression of mammalian antioxidant enzymes as well as to enhance numerous transcription factors, including nuclear factor kappaB, stress-activated protein kinase and heat shock factor This latter is the transcription factor for the synthesis of heat shock proteins, which have been known to protect against a wide variety of toxic conditions, including extreme temperatures, oxidative stress and cytotoxic drugs. In this study we investigated the role of oxidative stress in the induction of heat shock protein (HSP) 70 in human skin fibroblasts and the effect of vitamin E. We found that significant HSP70 induction occurred after exposure to HOOH and that this was associated with a significant perturbation in protein and nonprotein sulfhydryl groups, and with a significant increase in protein carbonyl levels. Treatment with vitamin E conferred significant protection against stress-induced modifications of cellular sulfhydryl and carbonyl content, while maintaining functional levels of cytoprotective HSP70. Our results point to the possible involvement of redox mechanisms in the heat shock signal transduction pathway, which may play an important regulatory role in the genetic mechanisms of tolerance to oxidative stress. Exogenous antioxidant supplementation with vitamin E could have cosmetic benefits and may be an efficient tool to mitigate the consequences of free radical-induced skin damage.
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PMID:Regulation of heat shock protein synthesis in human skin fibroblasts in response to oxidative stress: role of vitamin E. 1177 76

It is generally accepted that one of the major and important contributions to skin aging, skin disorders, and skin diseases results from reactive oxygen species. More than other tissues, the skin is exposed to numerous environmental chemical and physical agents, such as ultraviolet light, causing oxidative stress. Accelerated cutaneous UV-induced aging, photo aging, is only one of the harmful effects of continual oxygen radical production in the skin. Interestingly, our ELISA assays of 8-oxo-2'-deoxyguanosine in skin of young and old Balb/c mice showed that cumene hydroperoxide-induced accumulation of the biomarker of oxidative DNA damage in skin of 32-week-old mice occurred independently of their vitamin E status, while no accumulation of oxo8-dG was detectable in the skin of young animals. This suggests that vitamin E is not the major protector of skin against cumene hydroperoxide-induced oxidative stress. Production and accumulation of apoptotic cells is one of the characteristic features of skin damage by oxidative stress that, in the absence of effective scavenging by macrophages, dramatically enhances oxidative damage and inflammatory response. In our model experiments, we demonstrated that Cu-OOH induces significant oxidative stress in phospholipids of normal human epidermal keratinocytes (NHEK) whose characteristic feature is an early and profound oxidation of phosphatidylserine (PS), likely related to PS externalization. Since externalized PS is a signal for recognition of apoptotic cells by macrophage scavenger receptors, PS oxidation may be translatable into elimination of thus damaged NHEKs. Experiments are now underway to determine whether inhibition of PS oxidation by antioxidants may interfere with important signaling functions of oxidative stress in eliminating apoptotic cells.
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PMID:Toward mechanism-based antioxidant interventions: lessons from natural antioxidants. 1197 96

Few studies have indicated the use of antioxidants in the protection against cancers. The goal of this study was to develop a tissue culture model using MRC-5 cells, which would allow for rapid testing of treatments for skin damage, mediated by exposure to ultraviolet radiation (UVR). Overall the specific aims were to evaluate the morphological and pathophysiological responses of MRC-5 fibroblast cells exposed to UVR and antioxidant supplementation. In the first phase, MRC-5 cells were exposed to UVR for 30, 45 or 60 minute time intervals, and cellular damage was assessed biochemically and morphologically. In the second phase, cells were treated for 45 minutes in the presence or absences of physiological levels of vitamin E. The cells were evaluated after 24, 48, and 72 hours for biochemical and morphological changes. Structural changes were noted throughout the experimental phase among the UVR exposed groups compared with native control. However, treatment with vitamin E pre and post exposure provided a protective role by demonstrating lower levels of MDA (p < 0.05) as well as normal structural appearance.
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PMID:The effects of vitamin E on the proliferation and viability of irradiated fibroblast-like cells. 1208 62

The goal of this study was to develop a tissue culture model with and without cellular protection (anti-oxidants) in an attempt to prevent or treat squamous damage as a result of free radical generation. The specific aim was to evaluate the morphological responses of MRC-5 fibroblast cells exposed to UV-radiation and vitamin E supplementation. The criteria for the morphological evaluation was as follows; cell and nucleus shapes, size, N/C ratio, nucleus pleomorphism, hydropic swelling, as well as other features or characteristics of membrane and cytoplasmic alterations. The experimental design was divided into two phases. In the first phase the cells were exposed to radiation for 30, 45 and 60-minute intervals, the morphological evaluation was assessed using Image Pro Digital Analysis technique. In the second phase, vitamin E was administered to the cells before and after exposure to 45 min of radiation. Data obtained demonstrated that, forty-five minutes of radiation exposure caused traumatic stress to the cells, swelling, cellular debris and fragmentation. However, treatment with vitamin E pre and post exposure provided protection for the cells. Vitamin E treatment resulted in less cellular aggregation, more abundant eosinophilic cytoplasm and an overall healthy appearance. The data suggest that the use of vitamin E may minimize skin damage by protecting the integrity of the fibroblast cells for up to 72 hours in culture.
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PMID:Morphometric analysis of MRC-5 fibroblast like cells exposed to intermittent UV radiation. 1272 29

DNA damage caused by ultraviolet (UV) irradiation is considered the main etiologic factor contributing to the development of skin cancer. Systemic or topical application of antioxidants has been suggested as a protective measure against UV-induced skin damage. We investigated the effect of long-term oral administration of a combination of the antioxidants ascorbic acid (vitamin C) and D-alpha-tocopherol (vitamin E) in human volunteers on UVB-induced epidermal damage. The intake of vitamins C and E for a period of 3 mo significantly reduced the sunburn reaction to UVB irradiation. Detection of thymine dimers in the skin using a specific antibody revealed a significant increase of this type of DNA damage following UVB exposure. After 3 mo of antioxidant administration, significantly less thymine dimers were induced by the UVB challenge, suggesting that antioxidant treatment protected against DNA damage.
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PMID:Ultraviolet B-induced DNA damage in human epidermis is modified by the antioxidants ascorbic acid and D-alpha-tocopherol. 1567 47

Trichloroethylene (TCE) and perchloroethylene (PERC), the most common alkenyl halides, have been extensively used in industry, and can cause skin damage. To evaluate their cytotoxic potential on skin, the effects of these agents on the normal human epidermal keratinocytes (NHEK) were investigated. Their action on cell viability, membrane integrity and lipid peroxidation (LPO) was assessed by neutral red uptake (NRU) assay, lactate dehydrogenase (LDH) release test and measurement of malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity. In addition, the protective effect of antioxidatant vitamin E on the cytotoxicity was also studied. Incubation of NHEK with various concentrations (0.01-31.6 mM) of TCE or PERC caused a dose-dependent decrease in cell viability, with 80% reduction at 31.6 mM. NR50 values from the cytotoxicity assay was found to be 4.53 and 2.16 mM for TCE and PERC, respectively. A time- and concentration- dependent release of LDH were observed at 1, 2, 3, 4 h after cells were exposed to different doses of TCE or PERC. These agents also caused an increase of MDA, whilst an inhibition of SOD activity, in a concentration-dependent manner. Pre-treatment of the cells with vitamin E at 10-200 mM dose-dependently attenuated the cytotoxic effect of TCE or PERC. Pre-treatment with vitamin E also reversed subsequent TCE or PERC-induced release of LDH, elevation of lipid peroxidation and decline of anti-oxidant enzyme activities. These results suggest that TCE and PERC could induce cytotoxicity to NHEK associated with oxidative stress and antioxidatant vitamin E could effectively protect NHEK from TCE- or PERC-induced cytotoxicity, which may be associated to the superoxide scavenging effect and enhancement of anti-oxidant enzyme activities.
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PMID:Cytotoxicity of trichloroethylene and perchloroethylene on normal human epidermal keratinocytes and protective role of vitamin E. 1572 14

Background information on the inefficacy of sunscreens to provide free radical protection in skin, despite their usefulness in preventing sunburn/erythema, prompted us to synthesize a compound which would display in the same molecule both UV-absorbing and antioxidant capacities. For this purpose, the UVB absorber, 2-ethylhexyl-4-methoxycinnamate (OMC) was combined with the piperidine nitroxide TEMPOL, which has antioxidant properties. The spectral properties of the new nitroxide-based sunscreen (MC-NO) as well as its efficacy to prevent photo-oxidative damage to lipids induced by UVA, natural sunlight and 4-tert-butyl-4-methoxydibenzoylmethane (BMDBM), a photo-unstable sunscreen which generates free radicals upon UV radiation, was studied. The results obtained demonstrate that MC-NO: (a) absorbs in the UVB region even after UVA irradiation; (b) acts as free radical scavenger as demonstrated by EPR experiments; (c) strongly reduces both UVA-, sunlight- and BMDBM-induced lipid peroxidation in liposomes, measured as reduced TBARS levels; and (d) has comparable antioxidant activity to that of commonly used vitamin E and BHT in skin care formulations. These results suggest that the use of the novel sunscreen-antioxidant or of other nitroxide-based sunscreens in formulations aimed at reducing photoinduced skin damage may be envisaged.
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PMID:Synthesis and application of a novel sunscreen-antioxidant. 1655 75


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