Hiring in life sciences? Share your open positions with our professional community. Read more Close

Advertisement

Protective effects of naringenin and naringin against bisphenol A-induced male reproductive toxicity: mechanistic and preclinical evidence.

Created on 14 Oct 2026

Authors

Okon Michael Ben, Ugwu Okechukwu Paul-Chima, Idehen Charles Iyore, Olorunnisola Sinbad Olubukola, Mounmbegna Philippe, Aja Patrick Maduabuchi

Published in

Basic and clinical andrology. Volume 36. Issue 1. Oct 13, 2026. Epub Oct 13, 2026.

Abstract

Bisphenol A (BPA) has been associated with altered male reproductive hormones and semen endpoints in epidemiological studies and produces endocrine, oxidative, mitochondrial, apoptotic, and developmental injury in experimental models. This narrative review evaluates BPA-specific evidence for naringenin and naringin separately from supportive evidence in other reproductive stress models. It also distinguishes directly exposed F1 outcomes from transgenerational inheritance and links sperm endpoints to hormones, histology, and molecular measures. This narrative review synthesizes evidence published mainly between January 2019 through September 2026, while retaining older studies of direct mechanistic relevance. Evidence was identified through targeted searches of PubMed, Scopus-indexed sources, Google Scholar, and publisher databases and was organized by exposure timing, biological mechanism, model type, and reproductive endpoint. The strongest evidence for BPA-related male reproductive toxicity comes from convergent cellular and animal data supported by heterogeneous human observational studies. The strongest evidence for naringenin or naringin is preclinical and includes BPA-specific Sertoli-cell and rat models as well as related oxidative, metabolic, and phthalate stress models. Across the broader preclinical literature, the flavanones modify redox, mitochondrial, inflammatory, and steroidogenic endpoints, but differences in model, dose, route, and bioavailability prevent quantitative comparison. The evidence supports mechanistic research, not clinical supplementation, and exposure reduction remains the primary public-health approach.

PMID:
42870232
Bibliographic data and abstract were imported from PubMed on 14 Oct 2026.

Read full publication at:
Please sign in to see all details.

Advertisement

Stats

  • Community rating n/a 0 votes
  • Reviewers' rating n/a 0 votes
  • Your rating

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

  • Recommendations n/a n/a positive of 0 vote(s)
  • Views 5
  • Comments 0

Recommended by

  • No recommendations yet.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.

Advertisement