8-Hydroxy-2'-Deoxyguanosine Is Increased in Epidermal Cells of Hairless Mice after Chronic Ultraviolet B Exposure

Hattori, Yukari; Nishigori, Chikako; Tanaka, Tomoyuki; Uchida, Koji; Nikaido, Osamu; Osawa, Toshihiko; Hayashi, Hiroshi; Imamura, Sadao; Toyokuni, Shinya

doi:10.1111/1523-1747.ep12365625

Cited by 198 publications

(144 citation statements)

References 38 publications

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“…In a variety of tissues, 8-OHdG is used as a marker of oxidative stress-related DNA injury to the nuclei or mitochondria [22,23]. Diabetic patients have been shown to have higher concentrations of 8-OHdG in blood cells [53] and in the urine [54], as well as in muscle tissue [55].…”

Section: Discussionmentioning

confidence: 99%

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients

et al. 2002

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Impaired insulin secretion and insulin resistance are a characteristic feature of Type II (non-insulin-dependent) diabetes mellitus [1,2]. In spite of extensive studies on the pathophysiology of diabetes, islet pathology and its pathogenesis remain controversial.Classical studies using histochemical methods to identify endocrine cells have reported varying results, including the severe loss of beta cells [3], modest changes with amyloid deposition [4,5] and even no change of islet beta-cell population [6]. Immunohistochemical techniques for the identification of specific populations of islet endocrine cells, showed a nearly 50 % reduction in beta-cell volume density in European Type II non-obese diabetic patients compared with non-diabetic control subjects [7]. Other studies have reported a 24 % reduction of islet beta-cell area density, a 58 % increase in A cell area density and a deposition of amyloid that correlated with the severity of islet pathology [8]. In another study of European Type II diabetic patients, a separate research group has reported Diabetologia (2002) Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients Abstract Aims/hypothesis. We examined the pancreatic islet lesions in Japanese patients with Type II diabetes mellitus to determine if the damage was related to oxidative stress. Methods. Morphometric analyses were performed on immunostained sections of the tail portion of the pancreas from 14 diabetic and 15 non-diabetic patients. Amyloid deposition and oxidative stress-induced tissue damage were evaluated by Congo-red staining and immunostaining. Resistance to oxidative stress was assessed from immunostaining results for Cu, Zn-superoxide dismutase (SOD). Expression of (pro)insulin mRNA was assessed by in situ hybridisation. Results. The pancreas from diabetic patients had amyloid deposition in about 15 % of the islets, intensified reactions of 8-OHdG and HNE, as well as reduced expression of SOD. Islet volume density of beta cells and total beta-cell mass in the pancreas from diabetic patients were reduced by 22 % (p < 0.001) and 30 % (p < 0.05). Islet volume density and total mass of (pro)insulin mRNA-positive cells were similarly reduced in diabetic patients by 22 % (p < 0.001) and 39 % (p < 0.05), respectively. Islet volume density of A cells was increased by 20 % (p < 0.001) but total mass did not change. There were no changes in volume densities of islet, D and PP cells. Reduced beta-cell volume density correlated with increased positive staining of 8-OHdG. Conclusion/interpretation. Japanese Type II diabetic patients show a reduction of beta-cell mass and evidence of increased oxidative stress-related tissue damage that is correlated with the extent of the beta-cell lesions. [Diabetologia (2002) 45: 85±96]

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Section: Discussionmentioning

confidence: 99%

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients

et al. 2002

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“…Thymine dimer and 6-4PP monoclonal antibodies are commercially available (Kamiya Biomedical Company, Seattle, WA, USA). Monoclonal antibodies specific for oxidative DNA damage, such as 8-hydroxy-2%-deoxyguanosine and DNA single-strand breaks, have also been generated and utilized for studying the photobiology of the skin (2,53). The 8-hydroxy-2%-deoxyguanosine antibody is commercially available (Genox Corporation, Baltimore, MD, USA).…”

Section: Monoclonal Antibodiesmentioning

confidence: 99%

“…Sunlight generates various types of DNA damage such as DNA photoproducts and oxidative DNA damage (1,2). More than 90% of the damage elicited by sunlight in the DNA of cultured cells is photoproducts that are induced exclusively by an ultraviolet (UV)-B component of sunlight (3).…”

Section: Introductionmentioning

confidence: 99%

Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

Kobayashi

Katsumi

Imoto

et al. 2001

Pigment Cell Research

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The major types of DNA damage induced by sunlight in the scope. This latter method allows us to reconstruct three-diskin are DNA photoproducts, such as cyclobutane pyrimidine mensional images of nuclei containing DNA photoproducts and to simultaneously examine DNA photoproducts and hisdimers (CPDs), (6-4)photoproducts (6-4PPs) and Dewar isotology in multilayered epidermis. Using those techniques, one mers of 6-4PPs. A sensitive method for quantitating and can determine the induction and repair of these three distinct visualizing each type of DNA photoproduct induced by biologtypes of DNA photoproducts in cultured cells and in the skin ically relevant doses of ultraviolet (UV) or sunlight is essential to characterize DNA photoproducts and their biological efexposed to sublethal or suberythematous doses of UV or solar simulated radiation. As examples of the utility of these techfects. We have established monoclonal antibodies specific for niques and antibodies, we describe the DNA repair kinetics CPDs, 6-4PPs or Dewar isomers. Those antibodies allow one to quantitate photoproducts in DNA purified from cultured following irradiation of human cell nuclei and the photoprotective effect of melanin against DNA photoproducts in cultured cells or from the skin epidermis using an enzyme-linked immunosorbent assay. One can also use those specific antibodpigmented cells and in human epidermis. ies with in situ laser cytometry to visualize and measure DNA

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“…Immunohistochemical staining of skin specimens was performed using a monoclonal antibody specific for 8-OHdG (N45.1) (WAKO Chemicals, Osaka, Japan) according to the method described by Hattori et al [11].…”

Section: Immunohistochemistrymentioning

confidence: 99%

Advanced Glycation Endproducts Act as An Initiator of Skin Tumors in Mice

Ogata

Hasegawa

Nakamura

et al. 2006

J. Clin. Biochem. Nutr.

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Summary The role of advanced glycation endproducts (AGEs) as the initiator of tumor induction was investigated in SENCAR mice. Initiation with AGEs-modified bovine serum albumin (AGEs-BSA) increased both the incidence of tumor-bearing mice and the mean number of tumors per mouse. An immunohistochemical study revealed an increase in 8-hydroxy-2'-deoxyguanosine (8-OhdG) in nuclei of epidermal cells in the AGEs-BSA treated mice. Furthermore, a Salmonella mutagenicity test revealed that AGEs-BSA was mutagenic only in Salmonella TA104, a strain more sensitive to oxidative stress than other strains. These results suggest that AGEs are mutagenic through a mechanism associated with oxidative stress.

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8-Hydroxy-2'-Deoxyguanosine Is Increased in Epidermal Cells of Hairless Mice after Chronic Ultraviolet B Exposure

Cited by 198 publications

References 38 publications

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients

Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

Advanced Glycation Endproducts Act as An Initiator of Skin Tumors in Mice

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