Evidence map›Paper›PMID 42330172›Full record

ArticleJBRA assisted reproduction2026

Ameliorative Effects of Vitamin C on Heat Stress-Induced Testicular Dysfunction in Wistar Rats.

Damilare Rotimi, Adebanke Olaide Adesupo, Marvis Ayoola, Tomilola Debby Olaolu, Oluyomi Stephen Adeyemi

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Article in JBRA assisted reproduction, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Damilare RotimiDepartment of Biochemistry, Landmark University, Omu-Aran 251101, Nigeria.
Adebanke Olaide AdesupoDepartment of Biochemistry, Landmark University, Omu-Aran 251101, Nigeria.
Marvis AyoolaDepartment of Physical Medicine and Rehabilitation, University of Missouri, Columbia, MO, United States.
Tomilola Debby OlaoluTulane University, School of Medicine, Department of Pathology and Laboratory Medicine, New Orleans, Louisiana, 70112.
Oluyomi Stephen AdeyemiDepartment of Biochemistry, Medicinal Biochemistry & Toxicology Laboratory, Bowen University, Iwo 232101, Nigeria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo evaluate the effects of repeated heat exposure on testicular function and sperm quality in Wistar rats and to determine whether vitamin C mitigates heat stress-induced reproductive damage.

methodsTwenty-four Wistar rats were allocated to four groups and treated for 28 days: (i) control, (ii) heat exposure (40°C for 4 hours/day), (iii) vitamin C (50 mg/kg), and (iv) vitamin C plus heat exposure. Antioxidant status (superoxide dismutase, catalase, reduced glutathione), oxidative/nitrosative stress markers (malondialdehyde, nitric oxide), reproductive hormones (testosterone, follicle-stimulating hormone, luteinizing hormone), testicular function markers (alkaline phosphatase, acid phosphatase, glycogen, protein), testicular cortisol and cholesterol, histological structure, body and testis weights, and sperm parameters (concentration, total count, motility profile) were assessed.

resultsHeat exposure significantly reduced antioxidant defenses (superoxide dismutase, catalase, reduced glutathione), increased malondialdehyde and nitric oxide levels, and disrupted reproductive hormones (decreased testosterone with increased follicle-stimulating and luteinizing hormones). Heat stress also decreased alkaline and acid phosphatase activities, glycogen, and protein levels, increased testicular cortisol and cholesterol, induced histological damage, and reduced body and testis weights. Sperm quality was impaired, with lower sperm concentration, total count, and fast motility, and higher slow and non-motile sperm fractions. Vitamin C co-treatment partially attenuated these effects, improving catalase activity, Nrf-2 levels, glycogen, testosterone, alkaline and acid phosphatase, and lessened lipid peroxidation.

conclusionRepeated heat exposure induced oxidative stress, hormonal imbalance, impaired sperm quality, and structural testicular injury in Wistar rats. Vitamin C provided partial protection against heat-induced testicular dysfunction, supporting its potential role as an adjunct antioxidant strategy; further studies should evaluate additional antioxidants and include gene expression analyses to clarify mechanisms and fertility outcomes.

Indexed as

AntioxidantsAscorbic AcidHeat-Shock ResponseTesticular DiseasesTestisAnimalsMaleOxidative StressRatsRats, WistarSpermatozoaSperm MotilityAntioxidantsAscorbic AcidAscorbic acidclimate changefertilityoxidative stressthermal stress

Identifiers

PMID42330172
PMCPMC13318291

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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.