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Impact of Coenzyme Q10 Administration on Lead Acetate-Induced Testicular Damage in Rats
Open accessAbstract
Exposure to lead (Pb) causes multiorgan dysfunction including reproductive impairments. Here, we examined the protective effects of coenzyme Q10 (CoQ10) administration on testicular injury induced by lead acetate (PbAc) exposure in rats. This study employed four experimental groups (n=7) that underwent seven days of treatment as follows: control group intraperitoneally (i.p.) treated with 0.1 ml of 0.9% NaCl containing 1% Tween 80 (v:v), CoQ10 group that was i.p. injected with 10 mg/kg CoQ10, PbAc group that was i.p. treated with PbAc (20 mg/kg), and PbAc+CoQ10 group that was i.p. injected with CoQ10 2 h after PbAc. PbAc injection resulted in increasing residual Pb levels in the testis and reducing testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Additionally, PbAc exposure resulted in significant oxidative damage to the tissues on the testes. PbAc raised the levels of prooxidants (malondialdehyde and nitric oxide) and reduced the amount of endogenous antioxidative proteins (glutathione and its derivative enzymes, catalase, and superoxide dismutase) available in the cell. Moreover, PbAc induced the inflammatory response as evidenced by the upregulation of inflammatory mediators (tumor necrosis factor-alpha and interleukin-1 beta). Further, PbAc treatment induced apoptosis in the testicular cells, as indicated by an increase in Bax and caspase 3 expression, and reduced Bcl2 expression. CoQ10 supplementation improved testicular function by inhibiting Pb accumulation, oxidative stress, inflammation, cell death, and histopathological changes following PbAc exposure. Our findings suggest that CoQ10 can act as a natural therapeutic agent to protect against the reproductive impairments associated with PbAc exposure.
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“This is in line with Sumi et al. (2018) and Fatima et al. (2021) who stated that CoQ10 inhibited the activation of caspase-3 and the release of cytochrome c from mitochondria via stabilizing the mitochondrial membrane, thus preventing the release of apoptotic mediators.”
From Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle? (2023) · cites this paper as El-Khadragy et al. 2020
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Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle?
El-Bassouny, D. R., Mansour, A. A., Ellakkany, A. S., Ayuob, N. N., & AbdElfattah, A. A. (2023) · Histochemistry and Cell Biology · doi:10.1007/s00418-023-02205-5
Metadata
- Authors
- El-khadragy, M., Al-Megrin, W. A., AlSadhan, N. A., Metwally, D. M., El-Hennamy, R. E., Salem, F. E. H., Kassab, R. B., & Abdel Moneim, A. E.
- Affiliations
- Biology Department, Faculty of Science, Princess Nourah Bint Abdulrahman University, Riyadh 84428, Saudi Arabia
- Almaarefa University (SA)
- Zagazig University (EG)
- Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo 11795, Egypt
- Taibah University (SA)
- Al Baha University (SA)
- ORCID
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2020-06-03
- Volume
- 2020
- Pages
- 1-12
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC7290879
- OpenAlex
- W3033636297
- Cited by
- 56
- References
- 57
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 9 · 2023: 13 · 2022: 12 · 2021: 7 · 2020: 2
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Princess Nourah Bint Abdulrahman University
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Keywords
- coenzyme Q10, lead acetate, lead toxicity, testicular damage, oxidative stress, reproductive toxicity, antioxidant enzymes, inflammation, apoptosis, testosterone, luteinizing hormone, follicle-stimulating hormone, lead accumulation, neuroprotection
- MeSH terms
- Animals, Follicle Stimulating Hormone, Glutathione, Male, Nitric Oxide, Organometallic Compounds, RNA, Messenger, Testis, Testosterone, Tumor Necrosis Factor-alpha, Ubiquinone, Lipid Peroxidation, Rats, Wistar, bcl-2-Associated X Protein, Caspase 3, Interleukin-1beta
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