Evidence map›Paper›PMID 8013423›Full record

ReviewEnvironmental health perspectives1993

DNA lesions, inducible DNA repair, and cell division: three key factors in mutagenesis and carcinogenesis.

B N Ames, M K Shigenaga, L S Gold

Open access · diamondAbstract readReview
In one paragraph

Review in Environmental health perspectives, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 338 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Pharmacological Activity ofPharmaceuticals (Basel, Switzerland) · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Norepinephrine-Induced DNA Damage in Ovarian Cancer Cells.International journal of molecular sciences · 2020
    Article
  15. Alcohol Effects on Colon Epithelium are Time-Dependent.Alcoholism, clinical and experimental research · 2019
    Article
  16. Article
  17. Article
  18. Rlip depletion prevents spontaneous neoplasia in TP53 null mice.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

B N AmesDivision of Biochemistry and Molecular Biology, University of California, Berkeley 94720.
M K Shigenaga
L S Gold
University of California, Berkeley · US

Funding

VIROLOGY AND CHRONIC INFECTIONP30ES001896 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI SMITH, MARTYN T · 1985 to 2003
$4.7M
MUTAGENESIS AND CARCINOGENESISR35CA039910 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI AMES, BRUCE N · 1985 to 1998
–
NCI NIH HHS CA 39910NIEHS NIH HHS ESO1896
6 · The paper itself

Abstract

DNA lesions that escape repair have a certain probability of giving rise to mutations when the cell divides. Endogenous DNA damage is high: 10(6) oxidative lesions are present per rat cell. An exogenous mutagen produces an increment in lesions over the background rate of endogenous lesions. The effectiveness of a particular lesion depends on whether it is excised by a DNA repair system and the probability that it gives rise to a mutation when the cell divides. When the cell divides, an unrepaired DNA lesion has a certain probability of giving rise to a mutation. Thus, an important factor in the mutagenic effect of an exogenous agent whether it is genotoxic or non-genotoxic, is the increment it causes over the background cell division rate (mitogenesis) in cells that appear to matter most in cancer, the stem cells, which are not on their way to being discarded. Increasing their cell division rate increases mutation and therefore cancer. There is little cancer from nondividing cells. Endogenous cell division rates can be influenced by hormone levels, decreased by calorie restriction, or increased by high doses of chemicals. If both the rate of DNA lesions and cell division are increased, then there will be a multiplicative effect on mutagenesis (and carcinogenesis), for example, by high doses of a mutagen that also increases mitogenesis through cell killing. The defense system against reactive electrophilic mutagens, such as the glutathione transferases, are also almost all inducible and buffer cells against increments in active forms of chemicals that can cause DNA lesions. A variety of DNA repair defense systems, almost all inducible, buffer the cell against any increment in DNA lesions. Therefore, the effect of a particular chemical insult depends on the level of each defense, which in turn depends on the past history of exposure. Exogenous agents can influence the induction and effectiveness of these defenses. Defenses can be partially disabled by lack of particular micronutrients in the diet (e.g., antioxidants).

Indexed as

Cell DivisionDNA DamageDNA RepairAnimalsClone CellsDietFemaleHumansMaleMutagenesisMutationNeoplasms

Identifiers

PMID8013423
PMCPMC1519422
OpenAlexW2079194714

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.