Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antioxidant enzyme activities of cultured human foreskin fibroblasts, keratinocytes, and melanocytes from healthy black and Caucasian donors were measured and compared. Fibroblasts had more (p less than 0.05) peroxidase, catalase, glutathione peroxidase, and superoxide dismutase activity than keratinocytes. Keratinocytes had more (p less than 0.05) peroxidase, catalase, glutathione peroxidase, and superoxide dismutase activity than melanocytes. No differences in antioxidant enzyme activities were observed between the cells of any type taken from black or Caucasian people. Antioxidant enzyme activities may affect resistance to damage by oxidants induced by ultraviolet radiation and inflammation.
J Invest Dermatol 1991 Sep
PMID:Disparate antioxidant enzyme activities in cultured human cutaneous fibroblasts, keratinocytes, and melanocytes. 187 41

Scavenging mechanisms for persistent free radicals were investigated using nitroxide-type radicals as model compounds. The free radical reducing activity of a) isolated thioredoxin reductase, a flavin containing oxidoreductase, b) skin homogenates, and c) the epidermis of hairless mice was studied by electron spin resonance spectroscopy. In all three systems, reduction rates of different classes of nitroxide free radicals exhibited the following order: oxazolidinoxy greater than piperidinoxy greater than dihydropyrroloxy. The main reductant for piperidinoxy radicals in mouse skin homogenate is ascorbic acid. Other reducing activities were stimulated by NAD(P)H and could be inhibited by N-ethyl maleimide, suggesting involvement of thiol-dependent processes. Mammalian thioredoxin, a competitive inhibitor of nitroxide reduction by thioredoxin reductase, significantly stimulates nitroxide scavenging in skin homogenate. Thioredoxin reductase did not significantly participate in nitroxide reduction in skin homogenates. At the surface of mouse epidermis a cationic dihydropyrroloxy nitroxide, which was stable in the presence of mammalian thioredoxin reductase was readily reduced. The epidermal reduction was inhibited by zinc, N-ethyl maleimide, and by heat (70 degrees C, 5 min). At least for mouse epidermis, reduction of a variety of nitroxides is a complex phenomenon involving enzymatic and nonenzymatic mechanisms and cannot be used as a specific assay for an enzyme, e.g., thioredoxin reductase. The study indicates the epidermis contains an effective antioxidant system that scavenges ascorbate-sensitive piperidinoxy nitroxides as well as more reducing radicals exemplified by dihydropyrroloxy nitroxides.
J Invest Dermatol 1989 Nov
PMID:Free radical reduction mechanisms in mouse epidermis skin homogenates. 238 May 82

To clarify the role of catalase, an antioxidant enzyme, in response to UV irradiation, we compared the effects of irradiation on cytotoxicity, activities of antioxidant enzymes, total glutathione concentrations, lipid peroxidation and the rate of collagen synthesis in skin fibroblasts from a patient with acatalasaemia and in those from a normal individual. The cells were irradiated with UVA (6 and 12 J/cm2 or UVB (0.5 and 1 J/cm2). Cell survival curves after UV irradiation were similar in cells from both subjects. Although superoxide dismutase activity in acatalasaemia cells was higher than in the control cells before irradiation, after irradiation the activity decreased in acatalasaemia cells (76% with 12 J/cm2 UVA, 47% with 1 J/cm2 UVB), but remained unchanged in control cells. Total glutathione concentrations also decreased in acatalasaemia cells (60% with 12 J/cm2) in response to UVA irradiation, but remained unchanged in control cells. Lipid peroxidation did not increase significantly in either cell type. The rate of collagen synthesis decreased to a similar extent in response to UV exposure in the two cell types (60-80% with 8.2 J/cm2 UVA, 40-50% with 10 mJ/cm2 UVB). We conclude from the results of cytotoxicity and lipid peroxidation that although acatalasaemia cells were killed by hydrogen peroxide at low concentrations with a single UV exposure, catalase functions only to a small degree as an antioxidant enzyme. There remains the possibility, however, that a deficiency of catalase may chronically damage the skin resulting in a reduced defence function of superoxide dismutase and glutathione with repeated exposures to UV, which is becoming more common in our daily life.
Arch Dermatol Res 1995
PMID:Antioxidant defence mechanism of the skin against UV irradiation: study of the role of catalase using acatalasaemia fibroblasts. 855 87

Ultraviolet B radiation (UVB) induces oxidative damage in DNA, resulting in the formation of the adduct 8-hydroxydeoxyguanosine. Previous studies from this laboratory have demonstrated a decrease in antioxidant enzyme defenses after UVB radiation in Skh: HR-1 hairless mice, implicating antioxidant status in protection against oxidative damage. The present study was undertaken to examine mechanisms of UVB damage to DNA and modulation by vitamin C, selenite, or Trolox, a water-soluble vitamin E analog. BALB/c MK-2 mouse keratinocytes were exposed to a dose range of UVB from 4 to 750 mJ/cm2. DNA damage in the form of 80 HdG was measured using high-pressure liquid chromatography coupled with electrochemical and UV absorbance detection. Preincubation of the cells for 2 days with 0.4 or 0.8 microgram/ml ascorbic acid, 10 or 20 micrograms/ml Trolox, and 5 or 12.5 microM selenite resulted in a significant decrease in the number of 8-hydroxydeoxyguanosine adducts per 10(5) deoxyguanines induced by 500 mJ/cm2 UVB. The results indicate a potential role for antioxidant nutrients in protection against UVB damage to skin cells.
J Invest Dermatol 1996 May
PMID:Antioxidant nutrients protect against UVB-induced oxidative damage to DNA of mouse keratinocytes in culture. 861 44

Antioxidant enzyme activities in fibroblasts and erythrocytes prepared from normal and psoriatic patients were measured and compared. The most significant differences were noted in superoxide dismutase (SOD) activities. A dramatic (5.2-fold) increase in Mn-SOD activity along with a lesser (1.8-fold) increase in CuZn-SOD activity was observed in fibroblasts from lesional and nonlesional psoriatic skin. The increase of Mn-SOD activity was correlated with an increase of both protein and mRNA. A slight (1.2-fold) increase in CuZn-SOD activity was also found in psoriatic as compared to normal red blood cells, while Mn-SOD activity was not present in these cells. In contrast, both glutathione peroxidase and catalase activities were only slightly (1.3-fold) increased in psoriatic fibroblasts, with no appreciable change noted in psoriatic erythrocytes. Likewise, glutathione levels were observed to be similar in normal and psoriatic cells. The increases in SOD activities did not appear to correlate with the severity of the disease as expressed by the Psoriatic Area Severity Index score or with plasma inflammatory markers. These results demonstrate that antioxidant enzyme activities, particularly Mn-SOD in fibroblasts and CuZn-SOD in erythrocytes, are significantly elevated in cells from psoriatic patients.
J Invest Dermatol 1996 Jun
PMID:Antioxidant enzymes in psoriatic fibroblasts and erythrocytes. 875 78

Oxidative stress is known to be implicated in the inflammation induced by the anti-psoriatic irritant, dithranol. In this study, we wished to investigate whether this is reflected in the levels of the antioxidant enzyme, Cu,Zn-superoxide dismutase, as detected by quantitative immunocytochemistry, and whether similar changes also occur following exposure to an irritant not normally associated with reactive oxygen species generation, namely sodium lauryl sulphate. Analysis of biopsies from patch test sites revealed that significant reductions in the epidermal levels of Cu,Zn-superoxide dismutase were induced by both dithranol and sodium lauryl sulphate, although the time course of diminished activity was different for each irritant. Our findings suggest that oxidative stress plays a general role in the pathophysiology of acute irritant contact dermatitis.
Eur J Dermatol
PMID:Immunocytochemical demonstration of reduced Cu,Zn-superoxide dismutase levels following topical application of dithranol and sodium lauryl sulphate: an indication of the role of oxidative stress in acute irritant contact dermatitis. 964 16

Reactive oxygen species (ROS) play a role in the modulation of apoptosis. Antioxidant defence mechanisms against cell death involving apoptosis due to UVB irradiation were studied on three established cell lines (SCC derived from human skin squamous cell carcinoma, F-SV and F-ST derived from human skin fibroblasts) which were susceptible to cell death by UVB irradiation (12.5-250 mJ/cm2), and one cell line (N-F) derived from primary cultured human skin fibroblasts which was resistant to cell death. We compared antioxidant defences between the three established cell lines and N-F, measuring four antioxidant enzymes (superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and glutathione reductase (GR) and a non-enzymatic antioxidant glutathione. The greatest difference was that Cu, Zn-SOD activity in N-F was 3-4-times the three other cell lines. Though SCC had much larger amounts of glutathione and higher antioxidant enzyme activities except for Cu, Zn-SOD than N-F, SCC was very susceptible to cell death. After UVB irradiation (at 16 h after 12.5 mJ/cm2), in all cell lines, SOD activity increased 1.1-1.3-times that of non-irradiated cells, while other enzyme activities remained constant. This presumably represents a protective response against ROS generated during UVB irradiation. N-F which was resistant to UVB-induced cell death had higher Cu, Zn-SOD activity before UVB irradiation, and a larger increase of SOD (mainly Mn-SOD) after UVB exposure than the other cell lines which were susceptible to cell death. Therefore, we conclude that the most important enzymatic antioxidant to protect cells from UVB damage is SOD.
J Dermatol Sci 1998 Jun
PMID:Ultraviolet B-induced cell death in four cutaneous cell lines exhibiting different enzymatic antioxidant defences: involvement of apoptosis. 967 96

Chimeric epidermal reconstructs made with Negroid melanocytes and Caucasoid keratinocytes (or vice versa) were studied before and after UVB irradiation to understand the respective roles of these cells in tanning and photoprotection, especially lipoperoxidation and enzymatic defences against free radicals. Using this approach, we have confirmed overall the theory of the epidermal melanin unit. We have also shown that melanocytes of poorly tanning Caucasoids, which have a comparatively higher content of unsaturated fatty acids in their cell membrane, are more prone to the peroxidative effects of UV light, and that keratinocytes participate in photoprotection via phototype-dependent antioxidant enzyme activities, especially for catalase.
J Invest Dermatol 1998 Dec
PMID:Chimeric human epidermal reconstructs to study the role of melanocytes and keratinocytes in pigmentation and photoprotection. 985 24

In response to the attack of reactive oxygen species, the skin has developed a complex antioxidant defense system including among others the manganese-superoxide dismutase (MnSOD). MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen. We have addressed the question whether MnSOD is inducible upon UVA irradiation and whether repetitive UV exposure, as practiced for the light-hardening during phototherapy of various photodermatoses, can even enhance the adaptive antioxidant response. Single exposure of four different strains of fibroblasts to UVA irradiation resulted in a dose- and time-dependent increase in specific MnSOD mRNA levels. Interestingly, repetitive UVA exposure at days 1, 2, and 3 at a dose rate of 200 kJ per m2 resulted in a 5-fold induction of specific MnSOD mRNA levels following the third UVA exposure. Similar results were obtained for MnSOD activity. This adaptive response in terms of upregulation of the antioxidant enzyme MnSOD correlates with the protection against high UV doses, if cells were preexposed to sublethal UV doses. Importantly, MnSOD substantially differed between the tested individuals in both mRNA and activity levels. Taken together, we here provide evidence for the increasing induction of MnSOD upon repetitive UVA irradiation that may contribute to the effective adaptive UVA response of the skin during light hardening in phototherapy. Interindividual differences in the inducibility of MnSOD might account for differences in the susceptibility to develop photodermatologic disorders related to photosensitivity, photoaging, and skin cancer. The molecular basis for interindividual differences in the inducibility of antioxidant enzymes remains to be elucidated.
J Invest Dermatol 1999 Jan
PMID:Adaptive antioxidant response of manganese-superoxide dismutase following repetitive UVA irradiation. 988 57

It has been reported that cellular oxidative stress induces apoptosis. Ultraviolet radiation that generates reactive oxygen intermediates (ROIs) also induces apoptosis. Superoxide dismutase (SOD) is among the most active scavengers of ROIs, providing defense against the cellular oxidative stress. Mammalian cells express two isozymes of SOD, copper, zinc-SOD (Cu, Zn-SOD) and manganese-SOD (Mn-SOD). Using SV40-transformed human keratinocytes (SVHK cells), we investigated the role of SODs in the ultraviolet B (UVB) irradiation-induced apoptosis. UVB irradiation decreased transiently Cu, Zn- and Mn-SOD activities and their protein levels, with subsequent recovery to the basal levels by 24 h. The UVB-induced decrease in SOD activity was dose-dependent and the maximal effect was obtained at 75 mJ/cm(2). The decrease in Cu, Zn-SOD was more marked than that in Mn-SOD. The cell death assay, annexin-V/propidium iodide flow cytometry, and DNA fragmentation analysis revealed that UVB irradiation induces apoptosis in SVHK cells. The UVB-induced apoptosis was suppressed by the treatment of antioxidants, catalase, glutathione, and alpha-tochopherol. The stable transfection of Cu, Zn-SOD expression vectors into SVHK cells was accompanied by the increased activities of antioxidant enzymes, catalase, and glutathione reductase, as well as glutathione and the cells were shown to be more resistant to UVB-induced apoptosis. In contrast, the transfection of Mn-SOD affected neither activities of antioxidant enzymes nor the UVB-induced apoptosis. The transfection of Cu, Zn-SOD antisense oligomers but not sense oligomers into SVHK or Cu, Zn-SOD cDNA-transfected SVHK (C2) cells significantly decreased the antioxidant enzyme activities and increased the UVB-induced apoptosis. On the other hand, the transfection of Mn-SOD antisense oligomers did not affect the UVB-induced apoptosis. These results suggest that the transfection of Cu, Zn-SOD expression vector, which is accompanied by the increased level of antioxidant enzymes, suppresses the UVB-induced apoptosis of SVHK cells.
J Dermatol Sci 2000 May
PMID:Copper, zinc-superoxide dismutase protects from ultraviolet B-induced apoptosis of SV40-transformed human keratinocytes: the protection is associated with the increased levels of antioxidant enzymes. 1069 60


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