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Author

Ingrid Nordenson

Other affiliations: Lund University
Bio: Ingrid Nordenson is an academic researcher from Umeå University. The author has contributed to research in topics: Environmental exposure & Superoxide dismutase. The author has an hindex of 31, co-authored 66 publications receiving 3253 citations. Previous affiliations of Ingrid Nordenson include Lund University.


Papers
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Journal Article
TL;DR: An increased level of chromosome breakage appears to be a relevant biomarker of future cancer risk in peripheral blood lymphocytes, according to an ongoing Nordic cohort study of cancer incidence.
Abstract: Cytogenetic assays in peripheral blood lymphocytes (PBL) have been used extensively to survey the exposure of humans to genotoxic agents. The conceptual basis for this has been the hypothesis that the extent of genetic damage in PBL reflects critical events for carcinogenic processes in target tissues. Until now, no follow-up studies have been performed to assess the predictive value of these methods for subsequent cancer risk. In an ongoing Nordic cohort study of cancer incidence, 3182 subjects were examined between 1970 and 1988 for chromosomal aberrations (CA), sister chromatid exchange or micronuclei in PBL. In order to standardize for the interlaboratory variation, the results were trichotomized for each laboratory into three strata: low (1-33 percentile), medium (34-66 percentile), or high (67-100 percentile). In this second follow-up, a total of 85 cancers were diagnosed during the observation period (1970-1991). There was no significant trend in the standardized incidence ratio with the frequencies of sister chromatid exchange or micronuclei, but the data for these parameters are still too limited to allow firm conclusions. There was a statistically significant linear trend (P = 0.0009) in CA strata with regard to subsequent cancer risk. The point estimates of the standardized incidence ratio in the three CA strata were 0.9, 0.7, and 2.1, respectively. Thus, an increased level of chromosome breakage appears to be a relevant biomarker of future cancer risk.

510 citations

Journal ArticleDOI
TL;DR: The results fit the hypothesis that the increased rate of fetal deaths may be caused by genetic damage through occupational exposure of the husbands, however, carry-home exposure to the wives remains a possible alternative explanation.
Abstract: Among the wives of 764 workers at a copper smelter in northern Sweden there were no significant differences between pregnancies before and after the husband's occupational exposure, with respect to the rate of congenital malformations. The rate of fetal deaths was significantly increased in pregnancies after the husband's exposure (exposed pregnancies). No such increase was found among the wives of office workers. When background variables like smoking habits and alcohol consumption of the parents were studied, the rates of stillbirths and induced abortion were found to be associated with paternal alcohol consumption. Since many different relationships were tested, these associations may, however, be fortuitous. The rate of induced abortion was low and showed no difference between exposed and non-exposed pregnancies. In a second questionnaire series comprising persons who did not respond to the first questionnaire, there was a significantly increased rate of induced abortion. This result indicates that the willingness to cooperate in questionnaire studies of pregnancy outcome may be associated with previous pregnancy experience. The results fit the hypothesis that the increased rate of fetal deaths may be caused by genetic damage through occupational exposure of the husbands. However, carry-home exposure to the wives remains a possible alternative explanation.

195 citations

Journal ArticleDOI
TL;DR: The results indicate that SOD and possibly also CAT have a protective effect against arsenic-induced DNA damage and may be a synergist to ionizing radiation.
Abstract: Previous investigations have shown that trivalent arsenic is inducing chromosomal aberrations and sister chromatid exchanges (SCEs). In a search for the genotoxic mechanism we have studied the effects

137 citations

Journal ArticleDOI
TL;DR: Correlations were found between (chromosome and chromatid) breaks and gaps, which lends further support to the notion that gaps may be useful as indicators of genotoxic agents.
Abstract: A significantly increased frequency of chromosomal aberrations was found among lead-exposed workers at the Ronnskar smelter in northern Sweden. The frequency of aberrations showed a correlation with lead exposure as measured by the blood levels of lead. Strong individual variations were found. No synergistic effect of smoking was observed. Correlations were found between (chromosome and chromatid) breaks and gaps, which lends further support to the notion that gaps may be useful as indicators of genotoxic agents.

136 citations


Cited by
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01 Jan 2000
TL;DR: This annex is aimed at providing a sound basis for conclusions regarding the number of significant radiation accidents that have occurred, the corresponding levels of radiation exposures and numbers of deaths and injuries, and the general trends for various practices, in the context of the Committee's overall evaluations of the levels and effects of exposure to ionizing radiation.
Abstract: NOTE The report of the Committee without its annexes appears as Official Records of the General Assembly, Sixty-third Session, Supplement No. 46. The designations employed and the presentation of material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the United Nations concerning the legal status of any country, territory, city or area, or of its authorities, or concerning the delimitation of its frontiers or boundaries. The country names used in this document are, in most cases, those that were in use at the time the data were collected or the text prepared. In other cases, however, the names have been updated, where this was possible and appropriate, to reflect political changes. Scientific Annexes Annex A. Medical radiation exposures Annex B. Exposures of the public and workers from various sources of radiation INTROdUCTION 1. In the course of the research and development for and the application of atomic energy and nuclear technologies, a number of radiation accidents have occurred. Some of these accidents have resulted in significant health effects and occasionally in fatal outcomes. The application of technologies that make use of radiation is increasingly widespread around the world. Millions of people have occupations related to the use of radiation, and hundreds of millions of individuals benefit from these uses. Facilities using intense radiation sources for energy production and for purposes such as radiotherapy, sterilization of products, preservation of foodstuffs and gamma radiography require special care in the design and operation of equipment to avoid radiation injury to workers or to the public. Experience has shown that such technology is generally used safely, but on occasion controls have been circumvented and serious radiation accidents have ensued. 2. Reviews of radiation exposures from accidents have been presented in previous UNSCEAR reports. The last report containing an exclusive chapter on exposures from accidents was the UNSCEAR 1993 Report [U6]. 3. This annex is aimed at providing a sound basis for conclusions regarding the number of significant radiation accidents that have occurred, the corresponding levels of radiation exposures and numbers of deaths and injuries, and the general trends for various practices. Its conclusions are to be seen in the context of the Committee's overall evaluations of the levels and effects of exposure to ionizing radiation. 4. The Committee's evaluations of public, occupational and medical diagnostic exposures are mostly concerned with chronic exposures of …

3,924 citations

Journal ArticleDOI
Irwin Fridovich1
TL;DR: O2- oxidizes the [4Fe-4S] clusters of dehydratases, such as aconitase, causing-inactivation and release of Fe(II), which may then reduce H2O2 to OH- +OH..
Abstract: O2- oxidizes the [4Fe-4S] clusters of dehydratases, such as aconitase, causing-inactivation and release of Fe(II), which may then reduce H2O2 to OH- +OH.. SODs inhibit such HO. production by scavengingO2-, but Cu, ZnSODs, by virtue of a nonspecific peroxidase activity, may peroxidize spin trapping agents and thus give the appearance of catalyzing OH. production from H2O2. There is a glycosylated, tetrameric Cu, ZnSOD in the extracellular space that binds to acidic glycosamino-glycans. It minimizes the reaction of O2- with NO. E. coli, and other gram negative microorganisms, contain a periplasmic Cu, ZnSOD that may serve to protect against extracellular O2-. Mn(III) complexes of multidentate macrocyclic nitrogenous ligands catalyze the dismutation of O2- and are being explored as potential pharmaceutical agents. SOD-null mutants have been prepared to reveal the biological effects of O2-. SodA, sodB E. coli exhibit dioxygen-dependent auxotrophies and enhanced mutagenesis, reflecting O2(-)-sensitive biosynthetic pathways and DNA damage. Yeast, lacking either Cu, ZnSOD or MnSOD, are oxygen intolerant, and the double mutant was hypermutable and defective in sporulation and exhibited requirements for methionine and lysine. A Cu, ZnSOD-null Drosophila exhibited a shortened lifespan.

3,298 citations

Journal ArticleDOI
16 Aug 2002-Talanta
TL;DR: This review deals with environmental origin, occurrence, episodes, and impact on human health of arsenic, a metalloid occurs naturally, being the 20th most abundant element in the earth's crust.

3,166 citations

Journal ArticleDOI
25 Jan 1985-Science
TL;DR: Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents.
Abstract: There is convincing evidence that cellular prooxidant states--that is, increased concentrations of active oxygen and organic peroxides and radicals--can promote initiated cells to neoplastic growth. Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents. Many of these agents are promoters or complete carcinogens. They cause chromosomal damage by indirect action, but the role of this damage in carcinogenesis remains unclear. Prooxidant states can be prevented or suppressed by the enzymes of the cellular antioxidant defense and low molecular weight scavenger molecules, and many antioxidants are antipromoters and anticarcinogens. Finally, prooxidant states may modulate the expression of a family of prooxidant genes, which are related to cell growth and differentiation, by inducing alterations in DNA structure or by epigenetic mechanisms, for example, by polyadenosine diphosphate-ribosylation of chromosomal proteins.

2,488 citations

Journal ArticleDOI
TL;DR: A better understanding of the mechanism(s) of action) of arsenic will make a more confident determination of the risks associated with exposure to this chemical.

1,460 citations