Protective effects of melatonin on female rat ovary treated with nonylphenol

Göktepe, Özge; Balcıoğlu, Esra; Baran, Münevver; Özge, Cengiz; Ceyhan, Ayşe; Suna, Pınar Alisan; Bolat, Demet; Yalçın, Betül; Yay, Arzu

doi:10.1080/10520295.2022.2075566

Cited by 7 publications

(3 citation statements)

References 46 publications

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“…TGF-β1 signaling pathway plays an important role in the development of tissue fibrosis by induction expression of several pro-fibrotic genes, such as collagen I, collagen IV, integrin, and fibronectin [45]. In the present study, cisplatin-treated ovaries exhibited an increase in TGF-β1 mRNA expression together with increased collagen deposition in Masson's trichrome-stained ovarian tissue than that in normal controls [46][47][48].…”

Section: Discussionmentioning

confidence: 51%

Melatonin Mitigates Cisplatin-Induced Ovarian Dysfunction via Altering Steroidogenesis, Inflammation, Apoptosis, Oxidative Stress, and PTEN/PI3K/Akt/mTOR/AMPK Signaling Pathway in Female Rats

et al. 2022

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Ovarian damage and fertility impairment are major side effects of chemotherapy in pre-menopausal cancer patients. Cisplatin is a widely used chemotherapeutic drug. The present study was designed to assess the ameliorative effects of melatonin as an adjuvant for fertility preservation. Thirty-two adult female Wistar rats were divided randomly into four equal groups: Control, Melatonin, Cisplatin (CP) treated, and CP + Melatonin treated. The cisplatin-treated group showed decreased body and ovarian weights, decreased serum E2 and AMH, increased serum LH and FSH, reduced ovarian levels of SOD, CAT, GSH, and TAC, and increased ovarian MDA. The histopathological examination of the cisplatin-treated group showed deleterious changes within ovarian tissue in the form of damaged follicles and corpus luteum, hemorrhage, and inflammatory infiltrates with faint PAS reaction in zona pellucida, increased ovarian collagen deposition, and marked expression of caspase-3 immune reaction in granulosa and theca cells, stroma, and oocytes. Alongside, there was a significant downregulation in the mRNA expression of steroidogenic enzymes, IL10, AMPK, PI3K, AKT, mTOR, and PTEN, while TGF-β1, IL1β, IL6, TNF-α, NF-Kβ, P53, p38-MAPK, JNK, and FOXO3 mRNA expressions were upregulated in cisplatin-treated rats’ ovarian tissue. Coadministration of cisplatin-treated rats with melatonin reversed these changes significantly. In conclusion, melatonin’s antioxidant, anti-inflammatory, and anti-apoptotic activities could modulate ovarian disturbances induced by cisplatin and preserve fertility.

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Section: Discussionmentioning

confidence: 51%

Melatonin Mitigates Cisplatin-Induced Ovarian Dysfunction via Altering Steroidogenesis, Inflammation, Apoptosis, Oxidative Stress, and PTEN/PI3K/Akt/mTOR/AMPK Signaling Pathway in Female Rats

et al. 2022

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“…МТ, уменьшая окислительный стресс и апоптотическое повреждение, защищает клетки жёлтых тел в яичниках. Гормон восстанавливает пониженное в результате токсических воздействий количество жёлтых тел и численную плотность фолликулов у мышей и крыс [25,26], улучшает уровни лютеинизирующего гормона, лютеиновую функцию и выживаемость эмбрионов овец и коз [19]. МТ защищает жёлтое тело от АФК и играет ключевую роль в поддержании его функции у женщин [19].…”

Section: Microphotographs Of Rat Ovarian Corpus Luteum On Day 14 Afte...unclassified

The effect of melatonin on the Bcl-2 and Bad proteins expression in ovarian corpus luteum cells after exposure to experimental hyperthermia

Michurina,

Kolesnikov,

Ishchenko

et al. 2024

Acta biomedica scientifica

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Background. There is growing interest in determining the role of melatonin in the regulation of proliferation and apoptosis of ovarian cells at various diseases and destabilizing influences. It is believed that the choice between the implementation of a cell death or survival program determines the ratio of anti-apoptotic and pro-apoptotic proteins.The aim. To identify the effect ofmelatonin onthe expression ofanti-apoptotic Bcl-2 and pro-apoptotic Bad and the Bcl-2/Bad ratio in the ovarian luteocytes of Wistar rats in the acute (day 3) and recovery (days 7 and 14) periods after a single exposure to experimental hyperthermia.Methods. Warming up took no more than 17 minutes. Melatonin was injected subcutaneously (0.1 mg in 0.2 ml of physiological solution) for 3 days after experimental hyperthermia. Comparison groups included rats with physiological solution injection (control) and animals after experimental hyperthermia + physiological solution injection. The Bad and Bcl-2 expression was determined immunohistochemically on days 3, 7 and 14 after experimental hyperthermia + physiological solution or melatonin injection.Results. On the day 3 after experimental hyperthermia, the effect of the hormone was not detected. A week after experimental hyperthermia + melatonin injection, the Bad expression area decreased more significantly than in rats after experimental hyperthermia + physiological solution injection, which led to an increase in Bcl-2/ Bad ratio. This indicated an increase in anti-apoptotic protection, blocking the development of the internal apoptosis pathway at this time. 2 weeks after experimental hyperthermia + physiological solution injection, the Bcl-2 area decreased more significantly than the Bad area. As a result, the Bcl-2/Bad ratio decreased almost 2-fold compared to the control group. This indicated the activation of the “mitochondrial branch” of luteocyte apoptosis. 2 weeks after experimental hyperthermia + melatonin injection, the Bad and Bcl-2 areas decreased synchronously, which restored Bcl-2/ Bad to control values.Conclusion. The melatonin injection after experimental hyperthermia shifts the ratio of Bcl-2/Bad expression areas towards an increase in anti-apoptotic Bcl2 already a week after the recovery period and promotes earlier normalization of Bcl-2/Bad to physiological levels (as early as 2 weeks after experimental hyperthermia + melatonin injection).

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“…Indeed, NAC helps to reduce oxidative stress by neutralizing hydrogen peroxide, which is only one of the chemicals contributing to oxidative stress. These data may also implicate the involvement of various stress in BTB injury upon cadmium exposure, such as HRI-responsive mitochondrial stress[32], ER stress[33], and DNA Damage Response[34]. However, these cellular processes share a common activity of inducing autophagy.…”

Section: Discussmentioning

confidence: 99%

Cadmium Disrupts Blood-Testis Barrier (BTB) via An Oxidative Stress-Dependent Autophagy in Prepubertal Rats

Man,

Du,

Huang

et al. 2024

Preprint

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Blood testis barrier (BTB) is an important target of cadmium (Cd) toxicology, but the mechanism underlying the Cd-induced impairment of BTB function remains fully elucidated. The mammalian target of rapamycin (mTOR) complex 2 (mTOR2) regulates BTB function via its effects on cellular junctions and the cytoskeleton of Sertoli cells. In this study, we investigated whether mTOR2 was involved in the effects of Cd exposure on BTB integrity. A Cd exposure modelin vivowas established in prepubertal male rats using a single intraperitoneal injection of Cadmium Chloride (CdCl2). A Cd exposure model of Sertoli cell was established using a CdCl2-treated TM4 cell line. The Acute cadmium exposure decreased the activity of mTOR2 signaling and adhesin proteins which is linked to the induction of oxidative stress-induced autophagy. In the presence of CdCl2, mTOR, the catalytic subunit of the mTOR2 complex, exhibits a reduction in levels of phosphorylation, accompanied by decreased adhesin proteins and Rictor, the key component of the mTOR2 complex. CdCl2treatment also drives a process of oxidative stress-induced autophagy, evidenced by alterations in cellular markers for oxidative stress and autophagy. Pharmaceutical inhibition of oxidative stress and/or autophagy alleviates the alternations in mTOR2 signaling and adhesin proteins upon CdCl2treatment in TM4, a Sertoli cell line. This work is the first to examine the effects of cadmium exposure on rictor/mTOR2 signaling pathways. Our results suggest that Cadmium might exert testicular toxicology via the perturbation in mTOR2 signaling, which can be associated with the cellular stress-related protolysis in Sertoli cells.

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Protective effects of melatonin on female rat ovary treated with nonylphenol

Cited by 7 publications

References 46 publications

Melatonin Mitigates Cisplatin-Induced Ovarian Dysfunction via Altering Steroidogenesis, Inflammation, Apoptosis, Oxidative Stress, and PTEN/PI3K/Akt/mTOR/AMPK Signaling Pathway in Female Rats

Melatonin Mitigates Cisplatin-Induced Ovarian Dysfunction via Altering Steroidogenesis, Inflammation, Apoptosis, Oxidative Stress, and PTEN/PI3K/Akt/mTOR/AMPK Signaling Pathway in Female Rats

The effect of melatonin on the Bcl-2 and Bad proteins expression in ovarian corpus luteum cells after exposure to experimental hyperthermia

Cadmium Disrupts Blood-Testis Barrier (BTB) via An Oxidative Stress-Dependent Autophagy in Prepubertal Rats

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