Citalopram Induces Reproductive Toxicity in Male Rats
Citalopram hydrobromide (CTL) has been shown to cause sexual dysfunction; however, its reproductive toxicity potential has not been sufficiently elucidated in men. Therefore, we aimed to clarify the toxic effects of CTL on the reproductive system of male rats. For this purpose, CTL was administered...
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Published in | Birth defects research Vol. 109; no. 7; p. 475 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
17.04.2017
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Subjects | |
Online Access | Get more information |
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Summary: | Citalopram hydrobromide (CTL) has been shown to cause sexual dysfunction; however, its reproductive toxicity potential has not been sufficiently elucidated in men. Therefore, we aimed to clarify the toxic effects of CTL on the reproductive system of male rats.
For this purpose, CTL was administered at 5, 10, and 20 mg/kg/day to rats orally for 28 days. Sperm concentration, motility, and morphology were investigated using a computer-assisted sperm analysis system, and sperm DNA damage was detected using a Comet assay. The testes were histopathologically examined. Serum follicle-stimulating hormone, luteinizing hormone, and testosterone levels were measured and the oxidative status of testes was investigated.
Our results showed that sperm concentration was reduced, and abnormal sperm morphology and sperm DNA damage were increased in CTL-administered groups. Additionally, histopathological changes were observed in the testes of CTL-administered rats. Luteinizing hormone levels were increased in CTL-administered groups, while testosterone levels were increased in the 5 and 10 mg/kg CTL-administered groups. Decreased glutathione signaled enhanced oxidative stress in the 10 and 20 mg/kg CTL-administered groups.
Thus, we concluded that CT induced testicular damage in male rats; this testicular damage was accompanied by oxidative stress and hormonal changes, which are considered as the important causes of reproductive disorders. Birth Defects Research 109:475-485, 2017. © 2017 Wiley Periodicals, Inc. |
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ISSN: | 2472-1727 |
DOI: | 10.1002/bdr2.1010 |