ArticleScientific reports2026
ATRA-mediated RAR-α activation attenuates acrylamide-induced testicular toxicity.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acrylamide (ACR) is an environmental reproductive toxicant with unclear testicular toxicity mechanisms. Retinoids are a group of vitamin A-related compounds that function by activating retinoid receptors. We aimed in this study to further explore All-trans retinoic acid's (ATRA) protective response against an acrylamide-induced testicular insult model and the underlying possible mechanisms. Fifty male rats were allocated into control, DMSO, ACR (40 mg/kg bwt, i.p. daily for 14 days), ATRA (7.5 mg/kg bwt, i.p. daily), and ACR + ATRA groups. Body and testes weights, sperm parameters, testosterone level, and lactate dehydrogenase-X (LDH-X) activity were measured. In addition, testicular levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), caspase-3, Bax, and Bcl-2 were determined. Also, tissues were examined for histopathologic changes and immune expression of retinoic acid receptor-alpha (RAR-α). ACR exposure led to reduced body and testicular weights, impaired sperm parameters, and suppressed reproductive hormones (testosterone, FSH, LH). Testicular LDH-X activity decreased, along with reduced testicular RAR-α expression. Oxidative stress resulted in GSH depletion, reduced CAT and SOD activities, and increased MDA. ACR also triggered inflammation and apoptosis, with elevated TNF-α, IL-1β, IL-6, caspase-3, Bax. In contrast, ATRA improved sperm parameters and levels of hormones, restored RAR-α expression, mitigated oxidative stress, and decreased inflammation and apoptosis markers. Morphometric and histopathologic studies supported these biochemical observations. Overall, RAR-α agonist (ATRA) is linked to attenuation against ACR-induced testicular damage, along with a reduction in oxidative stress, inflammation, and cell death. These findings suggest that retinoid signaling might serve as a possible therapeutic target for reproductive toxicities induced by ACR, necessitating further mechanistic exploration.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.