Evidence map›Paper›PMID 21373971›Full record

ArticleJournal of medical toxicology : official journal of the American College of Medical Toxicology2011

Gestational cadmium exposure-induced ovotoxicity delays puberty through oxidative stress and impaired steroid hormone levels.

Jawahar B Samuel, Jone A Stanley, Rajendran A Princess, Paulraj Shanthi, Maria S Sebastian

Open access · bronzeAbstract read
In one paragraph

Article in Journal of medical toxicology : official journal of the American College of Medical Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Prenatal metal mixtures and sex-specific infant negative affectivity.Environmental epidemiology (Philadelphia, Pa.) · 2021
    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

5 authors at 4 institutions in 2 countries.

Jawahar B SamuelDepartment of Zoology, St. John's College, Thirunelveli, TN, India. drbjsamuel@yahoo.co.in
Jone A Stanley
Rajendran A Princess
Paulraj Shanthi
Maria S Sebastian
St. John's College of Nursing · USSt. John's University · USSt. Xavier's College (Autonomous)Texas A&M University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium (Cd), an environmental pollutant, has been shown to be highly toxic to both humans and animals. Its widespread industrial use has led to its accumulation in the environment. Cd has been shown to target multiple organs following acute intoxication, causing nephrotoxicity, immunotoxicity, osteotoxicity, and reproductive toxicity. Cd can cross the placental barrier and cause a wide range of defects during fetal development. The current study was aimed to assess the effect of Cd on the female reproductive system. Female rats were exposed to Cd [50/200 ppm] from embryonic day 9 to 21 through drinking water. Serum steroid hormone concentrations, hematological parameters, antioxidant enzyme levels, and ovarian histopathology were described. Water consumption, gravid uterine/body weight decreased in both the doses of Cd-treated dams. The hematological parameters analyzed in rat pups showed a significant reduction in both doses of Cd studied, while hemoglobin showed a significant reduction in 200 ppm Cd treatment alone. MCHC levels did not show any variation in 50 ppm Cd treatment, while 200 ppm Cd treatment significantly increased. Specific activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and serum testosterone, estradiol, and progesterone were significantly decreased. The levels of hydrogen peroxide and lipid peroxidation were increased in 50 and 200 ppm Cd-treated rats. These changes were accompanied with disrupted ovarian histoarchitecture, an extended estrous cycle, and delayed pubertal onset in Cd-treated rats. The data generated from the present study suggest that gestational Cd treatment induces ovarian toxicity and reproductive dysfunction through increased oxidative stress.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsAntioxidantsBlood Cell CountBody WeightCadmiumEnzymesEstrous CycleFemaleHormonesHydrogen PeroxideLipid PeroxidationOrgan SizeOvarian DiseasesOvaryOxidative StressAntioxidantsCadmiumEnzymesHormonesHydrogen PeroxideReactive Oxygen SpeciesSteroids

Identifiers

PMID21373971
PMCPMC3550211
OpenAlexW2073633607

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.