Evidence map›Paper›PMID 37726447›Full record

ArticleBiological trace element research2024

Acetate Abates Arsenic-Induced Male Reproductive Toxicity by Suppressing HDAC and Uric Acid-Driven Oxido-inflammatory NFkB/iNOS/NO Response in Rats.

E E Besong, T M Akhigbe, J N Obimma, O O Obembe, R E Akhigbe

Abstract read
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Article in Biological trace element research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Fatty acids and epigenetics in health and diseases.Food science and biotechnology · 2024
    Review
  9. Article
  10. Cardiometabolic Disorder and Erectile Dysfunction.Cell biochemistry and biophysics · 2024
    Review
  11. Article
  12. Changes in SOD and NF-κB Levels inAntioxidants (Basel, Switzerland) · 2024
    Article
  13. Review
  14. Review
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 2 institutions in 1 country.

E E BesongDepartment of Physiology, Faculty of Basic Medical Sciences, Ebonyi State University, Abakaliki, Nigeria.
T M AkhigbeBreeding and Plant Genetics Unit, Department of Agronomy, Osun State University, Osogbo, Osun State, Nigeria.
J N ObimmaDepartment of Physiology, Faculty of Basic Medical Sciences, Ebonyi State University, Abakaliki, Nigeria.
O O ObembeDepartment of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, Osogbo, Osun State, Nigeria.
R E AkhigbeReproductive Biology and Toxicology Research Laboratory, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria. akhigberoland@gmail.com.
Ebonyi State University · NGOsun State University · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arsenic is associated with male reproductive toxicity through histone deacetylation and oxido-inflammatory injury. Notwithstanding, short-chain fatty acids such as acetate exert anti-oxido-inflammatory activities and inhibit histone deacetylation. This study investigated the impact of acetate on arsenic-induced male reproductive toxicity. Forty eight adult male Wistar rats were allotted into any of these four groups (n = 12 rats per group): vehicle-treated, sodium acetate-treated, arsenic-exposed, and arsenic-exposed + sodium acetate-treated. The results revealed that arsenic exposure prolonged the latencies of mount, intromission, and ejaculation and reduced the frequencies of mount, intromission, and ejaculation, as well as mating and fertility indices, litter size and weight, anogenital distance, anogenital index, and survival rate in male F1 offspring at weaning. Also, arsenic reduced the circulating levels of gonadotropin-releasing hormone, luteinizing hormone, follicle-stimulating hormone, and testosterone and testicular 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase activities. In addition, arsenic reduced the daily and total spermatid production, sperm count, motility, and viability but increased the percentage of sperm cells with abnormal morphology. Furthermore, arsenic increased testicular xanthine oxidase activity, uric acid, and malondialdehyde levels, and reduced glutathione content, superoxide dismutase and catalase activities, total antioxidant capacity, and Nrf2 level. More so, arsenic exposure increased testicular iNOS activity and nitric oxide (NO), TNF-α, IL-1β, IL-6, and NFkB levels as well as Bax, caspase 9, and caspase 3 activities, and reduced Bcl-2. These findings were associated with arsenic-induced increase in testicular arsenic concentration, histone deacetylase activity, and reduced testicular weight. Histopathological examination revealed that arsenic also disrupted testicular histoarchitecture, which was accompanied by altered testicular planimetry and reduced spermatogenic cells. Notwithstanding, sodium acetate alleviated arsenic-induced sexual dysfunction as well as biochemical and histological alterations. These were accompanied acetate-driven downregulation of histone deacetylase (HDAC) activity. Succinctly, acetate attenuated arsenic-induced male reproductive toxicity by suppressing HDAC and uric acid-driven oxido-inflammatory NFkB/iNOS/NO response.

Indexed as

ArsenicNF-kappa BNitric OxideRats, WistarUric AcidAcetatesAnimalsMaleNitric Oxide Synthase Type IIRatsReproductionTestisAcetatesArsenicNF-kappa BNitric OxideNitric Oxide Synthase Type IINos2 protein, ratUric AcidEnvironmental toxicantEpigeneticsHeavy metalsInfertilitySpermTestosterone

Identifiers

PMID37726447
OpenAlexW4386857270

What Socratic 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 Socratic graph.