Evidence map›Paper›PMID 42470492›Full record

ArticleMolecular biology reports2026

Investigating the effects of nicotinamide mononucleotide administration on testicular apoptosis, and mitochondrial function in doxorubicin-treated rats.

Paria Yousefi Khiabani, Reza Badalzadeh, Majid Shokoohi, Elnaz Zoghi, Alireza Alihemmati

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Article in Molecular biology 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.

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5 authors.

Paria Yousefi KhiabaniMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Reza BadalzadehMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID http://orcid.org/0000-0002-8092-7820
Majid ShokoohiClinical Research development unit of Tabriz Valiasr hospital, Tabriz University of Medical Sciences, Tabriz, Iran. majidshokoohi1994@gmail.com.ORCID https://orcid.org/0000-0001-5197-3740
Elnaz ZoghiDepartment of Clinical Pharmacy, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID http://orcid.org/0000-0001-5262-0218
Alireza AlihemmatiMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Hemmatti@yahoo.com.ORCID http://orcid.org/0000-0002-2929-006X

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6 · The paper itself

Abstract

backgroundMale infertility is one of the most important side effects of chemotherapy that can seriously compromise the quality of life of cancer patients. Doxorubicin, a widely used chemotherapy drug in the treatment of cancer patients, is known to cause testicular toxicity. Nicotinamide mononucleotide (NMN) has recently received attention due to its potential role in improving mitochondrial function and cellular resistance to oxidative stress. The aim of the present study was to investigate the protective effects of NMN on testicular apoptosis, inflammatory changes, oxidative stress, and mitochondrial function in rats treated with doxorubicin. MATERIAL AND

methodThirty-two male Wistar rats were randomly assigned into four groups: control, NMN, doxorubicin, and NMN + doxorubicin. NMN (100 mg/kg) was administered intraperitoneally for 28 days, whereas doxorubicin was injected intraperitoneally at a dose of 2 mg/kg every 48 h for 12 days (six injections; cumulative dose 12 mg/kg). Histopathological evaluation was performed using Johnson's scoring system and morphometric analysis of seminiferous tubules. Oxidative stress markers (MDA, SOD, and GPx), intracellular ROS levels, and mitochondrial membrane potential were assessed. In addition, Bax and Bcl-2 gene and protein expression were examined using RT-qPCR and Immunohistochemistry staining.

resultsDoxorubicin administration significantly decreased Johnson's score, seminiferous tubule diameter, epithelial thickness, antioxidant enzyme activity, and mitochondrial membrane potential, while markedly increasing ROS levels, lipid peroxidation, and Bax expression (p < 0.05). NMN treatment significantly attenuated these alterations by reducing oxidative stress and apoptosis while improving mitochondrial function and histological architecture of the testes.

conclusionNMN exerts significant protective impact against testicular damages related to doxorubicin via antioxidant, anti-apoptotic, and mitochondrial-protective mechanisms. These findings indicate that NMN attenuates structural and molecular indices of testicular injury induced by doxorubicin, although preservation of endocrine function and fertility potential remains to be established.

Indexed as

ApoptosisDoxorubicinMitochondriaNicotinamide MononucleotideTestisAnimalsInfertility, MaleMaleMembrane Potential, MitochondrialOxidative StressRatsRats, WistarReactive Oxygen SpeciesDoxorubicinNicotinamide MononucleotideReactive Oxygen SpeciesBaxBcl-2doxorubicinMitochondrial FunctionNMNoxidative stress

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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.