Effects of chronic amiodarone treatment on rat testis

Özkaya, Ahmet Kağan; Dilber, Embiya; Gürgen, Seren Gülşen; Kutlu, Ömer; Cansu, Ali; Gedik, Yusuf

doi:10.1016/j.acthis.2016.02.003

Cited by 6 publications

(2 citation statements)

References 34 publications

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“…At the cellular level, three pathological viewpoints (spermatogonial swelling, cytoplasmic vacuolation, and deformation of cellular architecture) were estimated on a semiquantitative scale from + to +++ according to their degrees. 36 …”

Section: Methodsmentioning

confidence: 99%

Sertraline-induced reproductive toxicity in male rats: evaluation of possible underlying mechanisms

et al. 2017

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This study was conducted to clarify the toxic effects of sertraline (SRT) on the reproductive system of male rats and to elucidate the underlying mechanisms. Rats were treated orally with SRT at doses of 5, 10, and 20 mg kg−1 for 28 consecutive days. At the end of the treatment period, sperm concentration, sperm motility, and sperm morphology were investigated by computer-assisted sperm analysis system whereas sperm DNA damage was detected by comet assay. The oxidative status of the testes was investigated, and a histopathological examination was conducted. Serum testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) levels were measured to determine the effects of SRT on the spermatogenesis process. One-way ANOVA, post-hoc Dunnett's T3 test for the sperm comet assay, and post-hoc Tukey's test for the others were performed for statistical analysis. The results showed that SRT caused an increase in sperm DNA damage and induced histopathological lesions in all groups treated with SRT. There was abnormal sperm morphology and increased malondialdehyde (MDA) in the 10 mg kg−1 treatment group. More dramatic changes were observed in the 20 mg kg−1 treatment group. Decreased sperm count was accompanied by a significant increase in abnormal sperm morphology, DNA damage, and degeneration in cellular-tubular structures. Serum LH and testosterone levels were elevated in the 20 mg kg−1 treatment group. Decreased glutathione (GSH) and increased MDA were signs of enhanced oxidative stress (OS). In conclusion, SRT induced testicular toxicity in a dose-dependent manner and OS is suggested as a crucial mechanism.

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Section: Methodsmentioning

confidence: 99%

Sertraline-induced reproductive toxicity in male rats: evaluation of possible underlying mechanisms

et al. 2017

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“…Amiodarone has a unique structure that allows it to form free radicals in a high oxidative environment [36][37][38][39]. Radical formation potentially explains why amiodarone most commonly damages highly oxidative environments such as lung, liver, and thyroid [40].…”

Section: Discussionmentioning

confidence: 99%

Isolated Neutropenia: An Unexplored Side Effect of Amiodarone

Patel

2020

J Med Cases

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Amiodarone has been widely used for the treatment of various arrhythmias. It is a potent P450 inhibitor leading to interaction with many commonly prescribed drugs. Also, due to its long half-life, lipophilicity, and broad tissue distribution, it can cause a wide range of toxicities. A 62-year-old male with the unknown past medical history presented to the emergency department following a grand mal seizure. The patient initially presented with atrial flutter, which was controlled with beta blockers but was switched to amiodarone after 2 weeks when he developed atrial fibrillation with the rapid ventricular response. Approximately 1 month into his hospital stay, the patient developed severe isolated neutropenia. After ruling out other etiologies, amiodarone was withdrawn. The patient's absolute neutrophil count recovered 3 days after discontinuation of amiodarone.

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Amiodarone-Induced Retinal Neuronal Cell Apoptosis Attenuated by IGF-1 via Counter Regulation of the PI3k/Akt/FoxO3a Pathway

et al. 2016

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Amiodarone (AM) is the most effective antiarrhythmic agent currently available. However, clinical application of AM is limited by its serious toxic adverse effects including optic neuropathy. The purpose of this study was to explore the effects of AM and to assess if insulin-like growth factor-1 (IGF-1) could protect retinal neuronal cells from AM-induced apoptosis, and to determine the molecular mechanisms underlying the effects. Accordingly, the phosphorylation/activation of Akt and FoxO3a were analyzed by Western blot while the possible pathways involved in the protection of IGF-1 were investigated by application of various pathway inhibitors. The full electroretinogram (FERG) was used to evaluate in vivo effect of AM and IGF-1 on rat retinal physiological functions. Our results showed that AM concentration dependently caused an apoptosis of RGC-5 cells, while IGF-1 protected RGC-5 cells against this effect by AM. The protective effect of IGF-1 was reversed by PI3K inhibitors LY294002 and wortmannin as well as the Akt inhibitor VIII. AM decreased p-Akt and p-FoxO3a while increased the nuclear localization of FoxO3a in the RGC-5 cells. IGF-1 reversed the effect of AM on the p-Akt and p-FoxO3a and the nuclear translocation of FoxO3a. Similar results were obtained in primary cultured retinal ganglia cells. Furthermore, FERG in vivo recording in rats showed that AM decreased a-wave and b-wave of FERG while IGF-1 reversed the effects of AM. These data show that AM induced apoptosis of retinal neuronal cells via inhibiting the PI3K/Akt/FoxO3a pathway while IGF-1 protected RGC-5 cells against AM-induced cell apoptosis by stimulating this pathway.

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Effects of chronic amiodarone treatment on rat testis

Cited by 6 publications

References 34 publications

Sertraline-induced reproductive toxicity in male rats: evaluation of possible underlying mechanisms

Sertraline-induced reproductive toxicity in male rats: evaluation of possible underlying mechanisms

Isolated Neutropenia: An Unexplored Side Effect of Amiodarone

Amiodarone-Induced Retinal Neuronal Cell Apoptosis Attenuated by IGF-1 via Counter Regulation of the PI3k/Akt/FoxO3a Pathway

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