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Peer-reviewedCC BY 4.0Food & Nutrition Research

A dose-related miRNA panel reveals candidate tissue markers and potential mechanisms for sunset yellow-induced testicular toxicity

  • Mahintaj Dara1
  • Fatemeh Nazari2
  • Sanaz Alaee1,3
  • Zahra khodabandeh1,4
4 affiliations
  1. 1Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
  2. 2Department of Biology, Faculty of Science, Hakim Sabzevari University, Sabzevar, Iran
  3. 3Department of Reproductive Biology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran
  4. 4Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Amsterdam, the Netherlands
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Abstract

Background: Sunset Yellow (SY), a widely used azo dye food additive, has raised increasing health concerns. However, its potential testicular toxicity and the underlying molecular mechanisms, particularly those involving regulatory microRNAs (miRNAs), remain poorly understood.

Objective: This study aimed to investigate the effects of SY exposure on testicular histopathology and the expression patterns of key miRNAs (miR-34c, miR-122, and let-7a) in a rat model.

Design: Rats were exposed to low and high doses of SY for 28 days. Testicular tissues were analyzed using Hematoxylin and Eosin (H&E) and quantitative PCR for miRNA expression. Statistical analysis was performed to assess dose-dependent effects.

Results: SY exposure induced severe histopathological damage in a dose-dependent manner, including disrupted seminiferous tubule architecture, germ cell depletion, vacuolization, and interstitial cell changes. High-dose SY caused significant downregulation of miR-34c (P < 0.0001) and upregulation of miR-122 (16.2-fold, P < 0.0001), while let-7a showed alteration only at high doses. The miRNA expression changes showed a parallel association with the severity of histological impairment at the group level.

Conclusion: This study demonstrates that SY induces dose-related testicular toxicity via dysregulation of miR-34c and miR-122. These candidate tissue markers are associated with testicular damage and support risk assessment and regulatory strategies, although further mechanistic and validation studies are needed.

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Cite

BibTeXRIS
BibTeX
@article{dara2026doserelated,
  title = {{A dose-related miRNA panel reveals candidate tissue markers and potential mechanisms for sunset yellow-induced testicular toxicity}},
  author = {Mahintaj Dara and Fatemeh Nazari and Sanaz Alaee and Zahra khodabandeh},
  journal = {Food \& Nutrition Research},
  year = {2026},
  month = oct,
  doi = {10.29219/fnr.v70.14436},
  url = {https://doi.org/10.29219/fnr.v70.14436},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - A dose-related miRNA panel reveals candidate tissue markers and potential mechanisms for sunset yellow-induced testicular toxicity
AU  - Mahintaj Dara
AU  - Fatemeh Nazari
AU  - Sanaz Alaee
AU  - Zahra khodabandeh
PY  - 2026
DA  - 2026/10/26
JO  - Food & Nutrition Research
DO  - 10.29219/fnr.v70.14436
UR  - https://doi.org/10.29219/fnr.v70.14436
AB  - Background: Sunset Yellow (SY), a widely used azo dye food additive, has raised increasing health concerns. However, its potential testicular toxicity and the underlying molecular mechanisms, particularly those involving regulatory microRNAs (miRNAs), remain poorly understood.  Objective: This study aimed to investigate the effects of SY exposure on testicular histopathology and the expression patterns of key miRNAs (miR-34c, miR-122, and let-7a) in a rat model.  Design: Rats were exposed to low and high doses of SY for 28 days. Testicular tissues were analyzed using Hematoxylin and Eosin (H&E) and quantitative PCR for miRNA expression. Statistical analysis was performed to assess dose-dependent effects.  Results: SY exposure induced severe histopathological damage in a dose-dependent manner, including disrupted seminiferous tubule architecture, germ cell depletion, vacuolization, and interstitial cell changes. High-dose SY caused significant downregulation of miR-34c (P < 0.0001) and upregulation of miR-122 (16.2-fold, P < 0.0001), while let-7a showed alteration only at high doses. The miRNA expression changes showed a parallel association with the severity of histological impairment at the group level.  Conclusion: This study demonstrates that SY induces dose-related testicular toxicity via dysregulation of miR-34c and miR-122. These candidate tissue markers are associated with testicular damage and support risk assessment and regulatory strategies, although further mechanistic and validation studies are needed.
SN  - 1654-661X
ER  -