Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There has not as yet been an integrated, comprehensive study of the responses of dermis and epidermis in vivo to a wide range of ultraviolet (UV) doses, encompassing all major antioxidants and a sensitive marker of oxidative damage. We have irradiated hairless mice with simulated solar light at doses of 2, 5, 12.5, and 25 J/cm2 combined UVA and UVB (0.8 to 10 MED) and measured enzymic and non-enzymic antioxidants as well as lipid hydroperoxides in both epidermis and dermis to elucidate the response of cutaneous antioxidant defense mechanisms to UV stress. Among the nonenzymic antioxidants two different dose-response patterns were seen. Ascorbate was rapidly depleted at doses between 0 and 5 J/cm2 but was less affected between 5 and 25 J/cm2. In contrast, glutathione, ubiquinol/one, and alpha-tocopherol levels remained approximately equal to control levels between 0 and 5 J/cm2, then decreased to varying degrees from 5 to 25 J/cm2; ubiquinol was almost completely depleted, whereas alpha-tocopherol dropped only 30%. The concentration of lipid hydroperoxides increased throughout the dose range. These results may be explained partly by direct destruction of some antioxidants by UV light, partly by the separate antioxidant functions of the compounds, and partly by recycling of some antioxidants (e.g., alpha-tocopherol) at the expense of others (e.g., ubiquinol). Even at the lowest dose (0.8 MED) lipid hydroperoxide formation was observed. Among the enzymic antioxidants, superoxide dismutase activity decreased significantly (to 63.6% of initial activity for epidermis and 51.5% for dermis at 25 J), whereas activities of glutathione peroxidase and glutathione reductase decreased slightly. Catalase activity decreased dramatically at doses above 5 J (to 11.8% of initial activity in epidermis and 27.7% in dermis at 25 J). The dramatic loss of catalase is almost entirely accounted for by direct destruction by the simulated solar light, but superoxide dismutase was unaffected by direct exposure; hence its destruction must be due to indirect effects, either mediated by free radicals or other harmful species formed upon irradiation. At low doses of UV light many components of the cutaneous antioxidant system were damaged, whereas at high doses all components were damaged and some were almost completely destroyed.
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PMID:Dose-response effects of acute ultraviolet irradiation on antioxidants and molecular markers of oxidation in murine epidermis and dermis. 815 Nov 22

We measured enzymic and non-enzymic antioxidants in human epidermis and dermis from six healthy volunteers undergoing surgical procedures. Epidermis was separated from dermis by curettage and antioxidants were measured by high-performance liquid chromatography (HPLC) or standard spectrophotometric methods. The concentration of every antioxidant (referenced to skin wet weight) was higher in the epidermis than in the dermis. Among the enzymic antioxidants, the activities of superoxide dismutase, glutathione peroxidase, and glutathione reductase were higher in the epidermis compared to the dermis by 126, 61 and 215%, respectively. Catalase activity in particular was much higher (720%) in the epidermis. Glucose-6-phosphate dehydrogenase and isocitrate dehydrogenase, which provide reduced nicotinamide adenine dinucleotide phosphate (NADPH), also showed higher activity in the epidermis than the dermis by 111% and 313%, respectively. Among the lipophilic antioxidants, the concentration of alpha-tocopherol was higher in the epidermis than the dermis by 90%. The concentration of ubiquinol 10 was especially higher in the epidermis, by 900%. Among the hydrophilic antioxidants, concentrations of ascorbic acid and uric acid were also higher in the epidermis than in the dermis by 425 and 488%, respectively. Reduced glutathione and total glutathione were higher in the epidermis than in the dermis by 513 and 471%. Thus the antioxidant capacity of the human epidermis is far greater than that of dermis. As the epidermis composes the outermost 10% of the skin and acts as the initial barrier to oxidant assault, it is perhaps not surprising that it has higher levels of antioxidants.
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PMID:Enzymic and non-enzymic antioxidants in epidermis and dermis of human skin. 828 4

A comprehensive comparison of antioxidant defenses in the dermis and epidermis and their response to exposure to ultraviolet (UV) irradiation has not previously been attempted. In this study, enzymic and non-enzymic antioxidants in epidermis and dermis of hairless mice were compared. Enzyme activities are presented both as units/gram of skin and units/milligram of protein; arguments are presented for the superiority of skin wet weight as a reference base. Catalase, glutathione peroxidase, and glutathione reductase (units/gram of skin) were higher in epidermis than dermis by 49%, 86%, and 74%, respectively. Superoxide dismutase did not follow this pattern. Lipophilic antioxidants (alpha-tocopherol, ubiquinol 9, and ubiquinone 9) and hydrophilic antioxidants (ascorbic acid, dehydroascorbic acid, and glutathione) were 24-95% higher in epidermis than in dermis. In contrast, oxidized glutathione was 60% lower in epidermis than in dermis. Mice were irradiated with solar light to examine the response of these cutaneous layers to UV irradiation. After irradiation with 25 J/cm2 (UVA + UVB, from a solar simulator), 10 times the minimum erythemal dose, epidermal and dermal catalase and superoxide dismutase activities were greatly decreased. alpha-Tocopherol, ubiquinol 9, ubiquinone 9, ascorbic acid, dehydroascorbic acid, and reduced glutathione decreased in both epidermis and dermis by 26-93%. Oxidized glutathione showed a slight, non-significant increase. Because the reduction in total ascorbate and catalase was much more severe in epidermis than dermis, it can be concluded that UV light is more damaging to the antioxidant defenses in the epidermis than in the dermis.
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PMID:Antioxidant defense mechanisms in murine epidermis and dermis and their responses to ultraviolet light. 844 Sep 1

Oxidative stress parameters were evaluated in rat testes after chronic iron intoxication and vitamin E supplementation. Male Wistar rats were fed during 6 weeks with the following diets: C = rat chow; I = C + 25 mg carbonyl-iron/g diet; A = C + 0.2 mg alpha-tocopheryl acetate/g diet; and the combination of I and A (IA). After the treatment, no changes in final body weight, testis weight and protein content were observed. Total iron content in testes from the I group was 33% higher compared to the C group (216 +/- 10 nmol/g of tissue). The content of alpha-tocopherol (alphaT) was 2.5-fold higher in the A and IA groups compared to the C group (12.8 +/- 0.7 nmol/g tissue). The content of ubiquinol-9 (13.0 +/- 1.7 nmol/g tissue) and ubiquinol-10 (3.3 +/- 0.5 nmol/g tissue) was similar among the groups. Superoxide dismutase activity was 13 and 16% lower in the A and IA groups with respect to the C group (12.9 +/- 0.7 U/mg protein). Catalase activity was 26 and 33% lower in the I and IA groups than in the C (0.19 +/- 0.01 pmol/mg protein) and A (0.21 +/- 0.01 pmol/mg protein) groups, respectively. Glutathione peroxidase was 24 and 23% higher in the IA group than in the C (11.4 +/- 0.3 mU/mg protein) and I (11.5 +/- 1.0 mU/mg protein) groups, respectively. The testes content of 2-thiobarbituric acid-reactive substances (TBARS) and protein-associated carbonyl groups were 37 and 16% higher, respectively, in the I group than in the C group. These increased in TBARS and carbonyls, were not observed in the IA group. No diet-associated changes were observed in the steady state levels of 8-oxo-2'-deoxyguanosine in testes DNA (4.2 +/- 0.2 residue/10(5) dG). The present data suggest that this model of chronic iron overload produced a mild oxidative damage in rat testes that was partially prevented by alphaT supplementation.
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PMID:Oxidative stress in testes of rats subjected to chronic iron intoxication and alpha-tocopherol supplementation. 1043 81