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The potential protective role of coenzyme q10 on the cyclophosphamide-induced lung toxicity in adult male albino rats: a histological and ultrastructural study
Open accessAbstract
Background: Cyclophosphamide is anticancer and immunosuppressant agent used to treat malignant and autoimmune diseases. Its long-term use causes side effects, as infertility and pulmonary toxicity. Coenzyme Q10; the only synthesized antioxidant in human body, acts as powerful antioxidant, scavenging free radicals, and inhibiting lipid peroxidation. Aim of present study was to examine effect of coenzyme Q10 on blood biochemical profiles, histopathological changes in lungs of adult rats exposed to cyclophosphamide-induced toxicity. Methods: 36 adult male albino rats divided into four groups; control and three experimental each having 9 rats. First experimental group received coenzyme Q10, second received cyclophosphamide while third group received coenzyme Q10 along with cyclophosphamide. Experiment lasted for 7 days. On 8th day, animals were sacrificed by decapitation. Lung tissue samples were collected for histopathological examination. SOD (superoxide dismutase) and MDA (malondialdehyde) levels were determined and used for statistical analysis. Results: In coenzyme Q10 treated group, H&E stained sections revealed normal respiratory alveoli. Ultrathin sections revealed normal alveolar septa, pneumocyte and blood capillaries contain erythrocytes. In cyclophosphamide treated group, H&E stained sections revealed peribronchial and interstitial fibrosis. Ultrathin sections revealed alveoli having apparent free lumen with extravasated erythrocytes. Alveolar septa revealed collagen fibrils deposits, and proliferated fibroblasts. In combined coenzyme Q10 and cyclophosphamide treated group, H&E stained sections revealed marked decrease of inter-alveolar tissue thickening. Ultrathin sections revealed destructed alveolar septa with dissociated remnants of collagen fibrils. Blood capillaries appeared wide, containing monocytes and erythrocytes. Conclusions: Administration of coenzyme Q10 with cyclophosphamide is advised to alleviate cyclophosphamide-induced lung toxicity.
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“This was supported by other studies that have mentioned that the antifibrotic effect of CoQ10 could be due to altered profibrotic gene expression and ROS scavenging”
From Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle? (2023) · cites this paper as Olama et al. 2018
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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
“This was supported by other studies that have mentioned that the antifibrotic effect of CoQ10 could be due to altered profibrotic gene expression and ROS scavenging (Olama et al. 2018).”
Result
Metadata
- Authors
- Olama, N. K., Taha, M., & Rady, H. Y.
- Affiliations
- Ain Shams University (EG)
- Mansoura University (EG)
- Venue
- International Journal of Scientific Reports
- Publisher
- Medip Academy
- Published
- 2018-08-24
- Volume
- 4
- Issue
- 9
- Pages
- 225
- ISSN
- 2454-2156 (ISSN-L)
- 2454-2164
- OpenAlex
- W2888124022
- Cited by
- 10
- References
- 27
- Citations by year
- 2024: 2 · 2023: 4 · 2021: 2 · 2020: 2
- FWCI
- 0.36
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- International Journal of Scientific Reports (publishedVersion)
- Funders
- Ain Shams University
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Chemotherapy-induced organ toxicity mitigation
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Paraquat toxicity studies and treatments
- Keywords
- coenzyme Q10, cyclophosphamide, pulmonary toxicity, lung histopathology, lung ultrastructure, antioxidants, oxidative stress, superoxide dismutase, malondialdehyde, interstitial fibrosis, alveolar septa, drug-induced lung injury
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