Mutation Research/DNAging最新文献_第5页

Effect of dietary restriction on DNA repair and DNA damage 饮食限制对DNA修复和DNA损伤的影响

Mutation Research/DNAging Pub Date : 1993-12-01 DOI: 10.1016/0921-8734(93)90023-V

Vivian Haley-Zitlin , Arlan Richardson

引用次数: 61

Enhanced DNA repair in lymphocytes of Down syndrome patients: the influence of zinc nutritional supplementation 唐氏综合征患者淋巴细胞DNA修复增强:锌营养补充的影响

Mutation Research/DNAging Pub Date : 1993-08-01 DOI: 10.1016/0921-8734(93)90012-R

Mariella Chiricolo , Anna Rita Musa , Daniela Monti , Maria Zannoti , Claudio Franceschi

{"title":"Enhanced DNA repair in lymphocytes of Down syndrome patients: the influence of zinc nutritional supplementation","authors":"Mariella Chiricolo , Anna Rita Musa , Daniela Monti , Maria Zannoti , Claudio Franceschi","doi":"10.1016/0921-8734(93)90012-R","DOIUrl":"10.1016/0921-8734(93)90012-R","url":null,"abstract":"<div><p>Oral zinc supplementation is able to correct zinc deficiency and some immune defects present in Down's syndrome (DS), while other beneficial effects can be predicted because of the broad spectrum of biochemical pathways and the great variety of enzymes which depend on zinc bio-availability. To test if the maintenance of DNA integrity is also affected by zinc supplementation, DNA damage and repair after γ-radiation was studied by alkaline elution assay in phytohemagglutinin-stimulated lymphocytes from Down's syndrome children before and after an oral zinc supplementation given for 4 months to correct their immune defects.</p><p>In comparison with lymphocytes from normal children the DNA damage induction after ionizing radiation in DS lymphocytes both before and after zinc supplementation was normal. On the other hand, the rate of DNA repair in DS was highly and significantly accelerated before zinc treatment. After supplemenation with zinc sulfate, the DNA repair rate was consistently slowed down becoming similar to that of control subjects.</p><p>This is the first demonstration that a nutritional intervention in humans is apparently able to modify the biochemical steps which control the rate of DNA repair.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":"295 3","pages":"Pages 105-111"},"PeriodicalIF":0.0,"publicationDate":"1993-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(93)90012-R","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18692508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 43

Life span reduction and carcinogenesis in the progeny of rats exposed neonatally to 5-bromo-2′-deoxyuridine 新生儿暴露于5-溴-2 ' -脱氧尿苷的大鼠后代的寿命缩短和致癌作用

Mutation Research/DNAging Pub Date : 1993-08-01 DOI: 10.1016/0921-8734(93)90013-S

Vladimir N. Anisimov, Galina Yu. Osipova

{"title":"Life span reduction and carcinogenesis in the progeny of rats exposed neonatally to 5-bromo-2′-deoxyuridine","authors":"Vladimir N. Anisimov, Galina Yu. Osipova","doi":"10.1016/0921-8734(93)90013-S","DOIUrl":"10.1016/0921-8734(93)90013-S","url":null,"abstract":"<div><p>Outbred LIO rats were given subcutaneous injections (3.2 mg) of a synthetic analogue of thymidine, 5-bromo-2′-deoxyuridine (BrdUrd) on days 1, 3, 7 and 21 postnatally. At 3 months, the treated males and females were mated to generate F<sub>1</sub> progeny. The mean life span decreased by 31.6% and 9.1% in male rats and by 21.1% and 7.2% in female rats exposed to BrdUrd and in their offspring, respectively. Exposure to BrdUrd increased the aging rate of the rats and of their progeny. Age-related changes in the length of the estruc cycle and in the incidence of persistent estrus and/or anestrus were observed earlier in female rats exposed neonatally to BrdUrd and in their offspring compared to controls; also, developmental stigmas were observed in the offspring of rats exposed neonatally. The incidence of total and malignant tumors was increased in rats that had received BrdUrd as well as in their progeny. Our observations on the decrease in mean and maximum life span, the increase in aging rate, the acceleration of age-related changes in female reproductive system function, and the increase in tumor incidence and decrease in tumor latency in rats exposed to BrdUrd in early life suggest that this system could serve as a model of accelerated aging. These effects persist at least to the next generation.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":"295 3","pages":"Pages 113-123"},"PeriodicalIF":0.0,"publicationDate":"1993-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(93)90013-S","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18692509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Aphidicolin inhibits excision repair of UV-induced pyrimidine photodimers in low serum cultures of mitotic and mitomycin C-induced postmitotic human skin fibroblasts 在有丝分裂和丝裂霉素c诱导的有丝分裂后人皮肤成纤维细胞的低血清培养中，阿霉素抑制紫外线诱导的嘧啶光二聚体的切除修复

Mutation Research/DNAging Pub Date : 1993-08-01 DOI: 10.1016/0921-8734(93)90014-T

Hugo J. Niggli

{"title":"Aphidicolin inhibits excision repair of UV-induced pyrimidine photodimers in low serum cultures of mitotic and mitomycin C-induced postmitotic human skin fibroblasts","authors":"Hugo J. Niggli","doi":"10.1016/0921-8734(93)90014-T","DOIUrl":"10.1016/0921-8734(93)90014-T","url":null,"abstract":"<div><p>The rates of formation and excision of UVC light-induced cyclobutane-type pyrimidine photodimers were determined in cultures of foreskin-derived normal human fibroblasts in mitotic (MF) and mitomycin-C (MMC)-induced postmitotic fibroblasts (PMF). Characteristic morphological changes support the notion that MMC accelerates the differentiation pathway from MF to PMF. In cultures treated with aphidicolin, I am able to show that this inhibitor of α and/or δ polymerases significantly inhibits the repair of pyrimidine photodimers in foreskin-derived mitotic and MMC-induced postmitotic fibroblasts in low serum cultures (0.5%) following UVC irradiation. Over the concentration range of 0–2 μg/ml of aphidicolin, there is a strong concentration-dependent inhibition of repair in cells treated with 10 J/m<sup>2</sup> of UVC and incubated with aphidicolin during the post-incubation time (0–24 h). The results demonstrate that pyrimidine photodimers are repaired in low serum cultures by an α- and/or δ-polymerase-dependent pathway. These data also imply that the fibroblast differentiation system is a very useful tool to unravel the complex mechanisms of UV-induced DNA damage and repair.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":"295 3","pages":"Pages 125-133"},"PeriodicalIF":0.0,"publicationDate":"1993-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(93)90014-T","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18692953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Mitochondrial mutations, cellular instability and ageing: modelling the population dynamics of mitochondria 线粒体突变，细胞不稳定和衰老:线粒体种群动力学建模

Mutation Research/DNAging Pub Date : 1993-08-01 DOI: 10.1016/0921-8734(93)90011-Q

A. Kowald, T.B.L. Kirkwood

{"title":"Mitochondrial mutations, cellular instability and ageing: modelling the population dynamics of mitochondria","authors":"A. Kowald, T.B.L. Kirkwood","doi":"10.1016/0921-8734(93)90011-Q","DOIUrl":"10.1016/0921-8734(93)90011-Q","url":null,"abstract":"<div><p>All eukaryotic cells rely on mitochondrial respiration as their major source of metabolic energy (ATP). However, the mitochondria are also the main cellular source of oxygen radicals and the mutation rate of mtDNA is much higher than for chromosomal DNA. Damage to mtDNA is of great importance because it will often impair cellular energy production. However, damaged mitochondria can still replicate because the enzymes for mitochondrial replication are encoded entirely in the cell nucleus. For these reasons, it has been suggested that accumulation of defective mitochondria may be an important contributor to loss of cellular homoeostasis underlying the ageing process.</p><p>We describe a mathematical model which treats the dynamics of a population of mitochondria subject to radical-induced DNA mutations. The model confirms the existence of an upper threshold level for mutations beyond which the mitochondrial population collapses. This threshold depends strongly on the division rate of the mitochondria. The model also reproduces and explains (i) the decrease in mitochondrial population with age, (ii) the increase in the fraction of damaged mitochondria in old cells, (iii) the increase in radical production per mitochondrion, and (iv) the decrease in ATP production per mitochondrion.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":"295 3","pages":"Pages 93-103"},"PeriodicalIF":0.0,"publicationDate":"1993-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(93)90011-Q","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18692955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 44

Cell division, chromosomal damage and micronucleus formation in peripheral lymphocytes of healthy donors: related to donor's age 健康供者外周血淋巴细胞细胞分裂、染色体损伤及微核形成:与供者年龄有关

Mutation Research/DNAging Pub Date : 1993-08-01 DOI: 10.1016/0921-8734(93)90015-U

Bani Bandana Ganguly

引用次数: 100

Aneuploidy in human lymphocytes: an extensive study of eight individuals of various ages 人类淋巴细胞的非整倍体:对8个不同年龄个体的广泛研究

Mutation Research/DNAging Pub Date : 1993-03-01 DOI: 10.1016/0921-8734(93)90003-L

Florence Richard , Alain Aurias , Jérôme Couturier , Anne-Marie Dutrillaux , Anne Flüry-Hérard , Michèle Gerbault-Seureau , Françoise Hoffschir , Eugénie Lamoliatte , Danielle Lefrançois , Martine Lombard , Martine Muleris , Marguerite Prieur , Michèle Ricoul , Laure Sabatier , Evani Viegas-Péquignot , Vitaly Volobouev , Bernard Dutrillaux

{"title":"Aneuploidy in human lymphocytes: an extensive study of eight individuals of various ages","authors":"Florence Richard , Alain Aurias , Jérôme Couturier , Anne-Marie Dutrillaux , Anne Flüry-Hérard , Michèle Gerbault-Seureau , Françoise Hoffschir , Eugénie Lamoliatte , Danielle Lefrançois , Martine Lombard , Martine Muleris , Marguerite Prieur , Michèle Ricoul , Laure Sabatier , Evani Viegas-Péquignot , Vitaly Volobouev , Bernard Dutrillaux","doi":"10.1016/0921-8734(93)90003-L","DOIUrl":"10.1016/0921-8734(93)90003-L","url":null,"abstract":"<div><p>Data on aneuploidy from a prospective study on a large number of lymphocyte metaphases (over 1000 in 72-h and 100 in 48-h cultures) per individual from eight healthy donors of various ages are reported. Chromosome losses were dependent on culture time, being significantly more frequent in 72-h than in 48-h cultures. All donors exhibited various degrees of aneuploidy which increased with age in women. This increase resulted essentially from X chromosome losses, as previously reported. Although the rate of aneuploidy limited to autosomes was similar in newborns and in adults, the distributions of the missing autosomes were different. In the two newborns studied, autosome aneuploidy was random. In the adults, a significant inverse correlation with autosome lenghts was observed. The inverse correlation between chromosome lenghts and losses may be explained by selective pressure against monosomic cells in the adults.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":"295 2","pages":"Pages 71-80"},"PeriodicalIF":0.0,"publicationDate":"1993-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(93)90003-L","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18685290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 60

Age-dependent increases of DNA adducts (I-compounds) in human and rat brain DNA 人类和大鼠脑DNA中DNA加合物(i -化合物)的年龄依赖性增加

Mutation Research/DNAging Pub Date : 1993-01-01 DOI: 10.1016/0921-8734(93)90007-P

Kurt Randerath , Kim L. Putman , Heinz H. Osterburg , Steven A. Johnson , David G. Morgan , Caleb E. Finch

引用次数: 58

Effects of aging and caloric restriction on the genotoxicity of four carcinogens in the in vitro rat hepatocyte/DNA repair assay 衰老和热量限制对体外大鼠肝细胞/DNA修复实验中四种致癌物遗传毒性的影响

Mutation Research/DNAging Pub Date : 1993-01-01 DOI: 10.1016/0921-8734(93)90008-Q

J.G. Shaddock , R.J. Feuers , M.W. Chou , R.A. Pegram , D.A. Casciano

{"title":"Effects of aging and caloric restriction on the genotoxicity of four carcinogens in the in vitro rat hepatocyte/DNA repair assay","authors":"J.G. Shaddock , R.J. Feuers , M.W. Chou , R.A. Pegram , D.A. Casciano","doi":"10.1016/0921-8734(93)90008-Q","DOIUrl":"10.1016/0921-8734(93)90008-Q","url":null,"abstract":"<div><p>The effects of aging and chronic caloric restriction (CR) on the genotoxicity of four carcinogens, representing four different classes of chemicals, in the in vitro rat hepatocyte/DNA repair assay were investigated. Hepatocyte cultures were isolated from young, middel-aged, and old male Fischer (F344) rats which were maintained on either an ad libitum (AL) or a CR diet (60% of AL). Hepatocyte cultures from old AL rats, treated with 2-acetylaminofluorene (2-AAF), aflatoxin B<sub>1</sub> (AFB<sub>1</sub>), 7,12-dimethylbenz[<em>a</em>]anthracene (DMBA) and dimethylnitrosamine (DMN), exhibited age-related decreases in DNA repair as compared to young AL rats. By contrast, cultures from young CR rats exhibited significant diet-related decreases in DNA repair with 2-AAF, AFB<sub>1</sub>, DMBA and DMN, when compared to results from young AL diet-fed rats. Old CR F344 rat derived cultures exhibited no significant age-related dose-dependent decrease in the DNA repair response with any of the chemicals tested. However, in cultures from old CR rats 10.0 μM AFB<sub>1</sub> produced an age-related decrease in DNA repair from the response observed in young CR rats. When hepatocytes were isolated from Aroclor 1254-induced rats, increases in DNA repair were observed. These data indicate an age- and diet-related decrease in DNA repair and/or DNA damage and suggest that this decrease is due to a decrease in metabolic activation of these carcinogens to genotoxic species.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":"295 1","pages":"Pages 19-30"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(93)90008-Q","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18680827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 20

Contrasting effects of SH-compounds on oxidative DNA damage: repair and increase of damage sh -化合物对氧化性DNA损伤的影响对比:损伤修复和损伤加重

Mutation Research/DNAging Pub Date : 1993-01-01 DOI: 10.1016/0921-8734(93)90006-O

M.V.M. Lafleur, J. Retèl

{"title":"Contrasting effects of SH-compounds on oxidative DNA damage: repair and increase of damage","authors":"M.V.M. Lafleur, J. Retèl","doi":"10.1016/0921-8734(93)90006-O","DOIUrl":"10.1016/0921-8734(93)90006-O","url":null,"abstract":"<div><p>The non-radical singlet oxygen (<sup>1</sup>O<sub>2</sub>) and the OH radical (<sup>.</sup>OH) are the major damaging oxidative species that can be generated inside cells during normal aerobic metabolism and by processes such as photosensitization. Both reactive oxygen species fulfill essential prerequisites to be a genotoxic agent. Due to their continuous production the represent and ever-present threat to all vital cellular molecules, especially DNA. As might be anticipated from the difference in character between these reactive species (non-radical versus radical) the pattern of DNA modifications caused by singlet oxygen is different from that produced by OH radicals. All cells possess an elaborate defense system against oxidative damage. This paper focuses mainly on the effect of thiols such as glutathione, which are thought to play a role as antioxidants. Under certain conditions thiols can repair chemically, probably by H-donation, some of the DNA damage caused by <sup>.</sup>OH; for instance breaks can be rather easily prevented in this way. This process will complete with fixation of damage by oxygen. However, there is ample evidence that H-atom donation does not always lead to ‘correct’ repair. Moreover under aerobic conditions thiyl peroxy radicals might increase DNA damage. Although the repair/fixation process could be examined in the case of <sup>1</sup>O<sub>2</sub> yet, it could be demonstrated that reactive species can be formed out of the reaction of thios with <sup>1</sup>O<sub>2</sub> capable of enhancing the number of DNA modifications such as 8-oxoguanine and single-strand breaks, probably arising from different pathways. Although it si quite clear that thiols are to some extent excellent antioxidants they possess unexpected properties which, depending on the conditions, can have genotoxic consequences.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":"295 1","pages":"Pages 1-10"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(93)90006-O","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18680298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 35