Melatonin protects against visible light-induced oxidative stress and promotes the implantation potential of mouse blastocyst in vitro

Shafiei, Golnaz; Moghani-Ghoroghi, Fatemeh; Miyan, Jaleel; Almasi, Majid; Kashani, Iraj Ragerdi; Nikzad, Hossein; Hosseini, Elaheh Seyed; Moshkdanian, Ghazaleh

doi:10.1016/j.rvsc.2022.12.003

Cited by 3 publications

(1 citation statement)

References 39 publications

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“…Additionally, exogenous MT treatment could promote the implantation potential of mouse blastocyst under visible light-induced oxidative stress [17,18]. In together, these results illustrate that MT may own a dual role (antioxidant and autophagy) to protect cells even individuals from harmful stimuli.…”

Section: Introductionmentioning

confidence: 75%

Melatonin alleviates palmitic acid–induced mitochondrial dysfunction by decreasing oxidative stress and enhancing autophagy combined in bovine endometrial epithelial cells

Wang,

Zhu,

Zhao

et al. 2024

Preprint

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Background: Negative energy balance (NEB) typically occurs in dairy cows after delivery, with those in high yielding being more likely to experience significant NEB. Such metabolic imbalance could cause ketosis, which is often accompanied by a decline in reproductive performance, but the molecular mechanism has not been fully elucidated. During excessive NEB, the body fat is extensively broken down, resulting in abnormal accumulation of non-esterified fatty acids (NEFA), represented by palmitic acid (PA), within the uterus. Such an abnormal accumulation has the potential to damage bovine endometrial epithelial cells (BEECs), while the molecular mechanisms underlying its involvement in the PA-induced injury of BEECs is poorly understood. Melatonin (MT) is recognized for its regulatory role in maintaining the homeostasis of mitochondrial reactive oxygen species (mitoROS). However, less is known about whether MT could ameliorate the damage of PA on BEECs and its molecular mechanism. Results: Our results demonstrated that 0.2 mM PA stress increased the level of cellular and mitochondrial oxidative stress. Further, we observed mitochondrial dysfunction, including an abnormal incidence of mitochondrial structure and respiratory function, reduction in mitochondrial membrane potential and mitochondrial copy number, which in turn induced apoptosis. Notably, we also found an upregulation of autophagy protein (PINK, Parkin, LC3B et al), however, the P62 protein was also increased. As we expected, 100uM MT pre-treatment attenuated PA-induced mitochondrial ROS and restored mitochondrial respiratory function. Meanwhile, pre-treated MT reversed the upregulation of P62 induced by PA and activate the AMPK-mTOR-Beclin-1 pathway, contributing to increase of autophagy and decline apoptosis. Conclusions: These findings indicate that PA could induce mitochondrial dysfunction and also enhance autophagy in BEECs. In addition, MT is hypothesized to not only reduce mitochondrial oxidative stress but also facilitate the clearance of damaged mitochondria through the regulation of autophagy pathways, thereby safeguarding the mitochondrial pool and promoting cellular viability. Our study helps better understand the molecular mechanism involved in excessive NEB's impact on the fertility outcomes of high yielding dairy cows.

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Section: Introductionmentioning

confidence: 75%

Melatonin alleviates palmitic acid–induced mitochondrial dysfunction by decreasing oxidative stress and enhancing autophagy combined in bovine endometrial epithelial cells

Wang,

Zhu,

Zhao

et al. 2024

Preprint

View full text Add to dashboard Cite

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Melatonin alleviates palmitic acid-induced mitochondrial dysfunction by reducing oxidative stress and enhancing autophagy in bovine endometrial epithelial cells

Wang,

Gong,

Heng

et al. 2024

J Animal Sci Biotechnol

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Background Negative energy balance (NEB) typically occurs in dairy cows after delivery. Cows with a high yield are more likely to experience significant NEB. This type of metabolic imbalance could cause ketosis, which is often accompanied by a decline in reproductive performance. However, the molecular mechanisms underlying NEB have yet to be fully elucidated. During excessive NEB, the body fat is extensively broken down, resulting in the abnormal accumulation of non-esterified fatty acids (NEFAs), represented by palmitic acid (PA), within the uterus. Such an abnormal accumulation has the potential to damage bovine endometrial epithelial cells (BEECs), while the molecular mechanisms underlying its involvement in the PA-induced injury of BEECs remains poorly understood. Melatonin (MT) is recognized for its regulatory role in maintaining the homeostasis of mitochondrial reactive oxygen species (mitoROS). However, little is known as to whether MT could ameliorate the damage incurred by BEECs in response to PA and the molecular mechanism involved. Results Analysis showed that 0.2 mmol/L PA stress increased the level of cellular and mitochondrial oxidative stress, as indicated by increased reactive oxygen species (ROS) level. In addition, we observed mitochondrial dysfunction, including abnormal mitochondrial structure and respiratory function, along with a reduction in mitochondrial membrane potential and mitochondrial copy number, and the induction of apoptosis. Notably, we also observed the upregulation of autophagy proteins (PINK, Parkin, LC3B and Ubiquitin), however, the P62 protein was also increased. As we expected, 100 μmol/L of MT pre-treatment attenuated PA-induced mitochondrial ROS and restored mitochondrial respiratory function. Meanwhile, MT pretreatment reversed the upregulation of P62 induced by PA and activated the AMPK-mTOR-Beclin-1 pathway, contributing to an increase of autophagy and decline apoptosis. Conclusions Our findings indicate that PA can induce mitochondrial dysfunction and enhance autophagy in BEECs. In addition, MT is proved to not only reduce mitochondrial oxidative stress but also facilitate the clearance of damaged mitochondria by upregulating autophagy pathways, thereby safeguarding the mitochondrial pool and promoting cellular viability. Our study provides a better understanding of the molecular mechanisms underlying the effect of an excess of NEB on the fertility outcomes of high yielding dairy cows.

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Polycystic Ovary Syndrome Pathophysiology: Integrating Systemic, CNS and Circadian Processes

Anderson

2024

Front. Biosci. (Landmark Ed)

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The conceptualization of polycystic ovary syndrome (PCOS) has primarily focused on hormonal alterations driven by changes within the hypothalamus and ovarian granulosa cells, with treatment by the contraceptive pill and weight loss. However, a growing body of data implicates wider systemic and central nervous system (CNS) changes in the pathoetiology and pathophysiology of PCOS, with consequent implications for targeted treatments. It is proposed that there is a significant role for night-time interactions of factors acting to regulate whether the rising level of cortisol over the night and during the morning cortisol awakening response (CAR) is able to induce the nuclear translocation of the glucocorticoid receptor (GR), thereby influencing how the immune and glial systems regulate cellular function in preparation for the coming day. Factors affording protection in PCOS also inhibit GR nuclear translocation including gut microbiome-derived butyrate, and pineal/local melatonin as well as melatonin regulated bcl2-associated athanogene (BAG)-1. A significant pathophysiological role in PCOS is attributed to the aryl hydrocarbon receptor (AhR), which shows heightened levels and activity in PCOS. The AhR is activated by ligands of many systemic processes, including white adipocyte-derived kynurenine, implicating obesity in the pathophysiological changes occurring in the hypothalamus and ovaries. AhR activation has consequences for the physiological function in the hypothalamic paraventricular nucleus, granulosa cells and adipocytes, partly mediated by AhR upregulation of the mitochondrial N-acetylserotonin/melatonin ratio, thereby decreasing melatonin availability whilst increasing local stress plasticity in the paraventricular nucleus. This article reviews in detail the wider systemic and CNS changes in PCOS highlighting interactions of local and pineal melatonergic pathway, gut microbiome-derived butyrate, white adipocyte-derived kynurenine, the hypothalamic paraventricular nucleus tanycytes/astrocytes, and the hypothalamus-pituitary-adrenal (HPA) axis driven glucocorticoid receptor activation in PCOS pathophysiology. This integrates a wide array of previously disparate data on the biological underpinnings of PCOS, including how PCOS associates with many other currently classified medical conditions, such as depression, bipolar disorder, type 1 diabetes mellitus and the autism spectrum. Numerous future research and treatment implications are detailed.

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Melatonin protects against visible light-induced oxidative stress and promotes the implantation potential of mouse blastocyst in vitro

Cited by 3 publications

References 39 publications

Melatonin alleviates palmitic acid–induced mitochondrial dysfunction by decreasing oxidative stress and enhancing autophagy combined in bovine endometrial epithelial cells

Melatonin alleviates palmitic acid–induced mitochondrial dysfunction by decreasing oxidative stress and enhancing autophagy combined in bovine endometrial epithelial cells

Melatonin alleviates palmitic acid-induced mitochondrial dysfunction by reducing oxidative stress and enhancing autophagy in bovine endometrial epithelial cells

Polycystic Ovary Syndrome Pathophysiology: Integrating Systemic, CNS and Circadian Processes

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