Role of inflammation and oxidative stress in the etiology of primary ovarian insufficiency

Ağaçayak, Elif; Görük, Neval Yaman; Küsen, Hakan; Başaranoğlu, Serdar; İçen, Mehmet Sait; Yıldızbakan, Ahmet; Yüksel, Hatice; Kalkanlı, Sevgi; Gül, Talip

doi:10.4274/tjod.00334

Cited by 34 publications

(34 citation statements)

References 33 publications

(31 reference statements)

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“…It is confirmed that oxidative stress index levels are elevated in primary ovarian insufficiency patients [ 16 ]. Moreover, previous literatures indicated that when ovary is exposed to some drugs related to oxidative stress, such as chemotherapeutic drugs, gamma irradiation, or polycyclic aromatic hydrocarbons, loss of primordial follicles is induced.…”

Section: Introductionmentioning

confidence: 91%

Protective effects of mangafodipir against chemotherapy-induced ovarian damage in mice

Qin

Iwase

Murase

et al. 2018

Reprod Biol Endocrinol

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BackgroundGiven the seriousness of chemotherapy-induced ovarian injury in female cancer patients, the preservation of fertility, including through the use of cryopreservation technology and pharmaceuticals, requires investigation. Previous studies have shown that damage to the ovaries is related to oxidative stress caused by anticancer drugs. Therefore, superoxide dismutase (SOD) may represent a key factor in the pharmacological protection of the ovaries. The aim of our study was to identify the effects of mangafodipir, a manganese chelate and SOD-mimetic, on suppression of apoptosis in granulosa cells and primordial follicle activation induced by anticancer drugs.MethodsCell viability assays using methyltrichlorosilane solutions and immunoblotting for cleaved caspase-3 were performed in in vitro experiments with the simultaneous addition of mangafodipir to human non-luteinized granulosa cell line (HGrC) cultures treated with hydrogen peroxide (H2O2), cisplatin, or paclitaxel. Count and morphological analyses of follicles at each developing stage in the ovaries and immunohistochemistry for cleaved caspase-3, Ki67 and 4-hydroxynonenal, a marker for oxidative stress, were also performed using mangafodipir-injected 6-week-old female ICR mice treated with cisplatin or paclitaxel. Further, mangafodipir was injected into 6-week-old female BALB/c mice inoculated with ES-2 to analyze whether mangafodipir inhibits the anti-tumor effects of cisplatin or paclitaxel treatment.ResultsMangafodipir attenuated apoptosis induced by H2O2 and anticancer drugs in vitro. Mangafodipir also decreased the expression of 4-hydroxynonenal and reduced cisplatin- and paclitaxel-induced apoptosis in granulosa cells in vivo. In addition, mangafodipir inhibited the loss of primordial follicles. Tumor xenograft studies in mice showed that mangafodipir did not affect anticancer drug antitumor effects.ConclusionsOxidative stress might be one of the mechanisms of cisplatin- and paclitaxel-induced the loss of primordial follicles. Mangafodipir can reduce cisplatin- and paclitaxel-induced apoptosis in granulosa cells and primordial follicle activation partially via its SOD activity. At the same time, mangafodipir might have other potential mechanisms to inhibit the activation of primordial follicles. Further, mangafodipir attenuated the ovarian damage caused by cisplatin and paclitaxel without affecting their antitumor activities. Mangafodipir, therefore, though its efficacy might be limited, may be a new option for the preservation of fertility during anticancer treatment.

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Section: Introductionmentioning

confidence: 91%

Protective effects of mangafodipir against chemotherapy-induced ovarian damage in mice

Qin

Iwase

Murase

et al. 2018

Reprod Biol Endocrinol

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“…Preceding the last menstrual period, women undergo perimenopause, which lasts 4 years on average [140] and involves gradual, but highly fluctuating withdrawal of E2 [141]. The cessation of ovarian hormone function during perimenopause is associated with rises in chronic low-grade inflammation, which has been shown to promote ovarian insufficiency [142], and to increase the risk for developing obesity, AD, and autoimmune disorders [143]. For instance, the incidence of RA increases with menopause [143], and MS-related symptoms worsen after menopause [144].…”

Section: Menopausementioning

confidence: 99%

Towards an understanding of women's brain aging: the immunology of pregnancy and menopause

Barth¹,

Lange²

2020

Preprint

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Women are at significantly greater risk of developing Alzheimer's disease and show higher prevalence of autoimmune conditions relative to men. Women's brain health is historically understudied, and little is therefore known about the mechanisms underlying epidemiological sex differences in neurodegenerative diseases, and how female-specific factors may influence women's brain health across the lifespan. In this review, we summarize recent studies on the immunology of pregnancy and menopause, emphasizing that these major immunological and hormonal transition phases may play a critical part in women's brain aging trajectories.

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“…The endocrine transition of the perimenopause to the post-menopause, while associated with loss of reproductive function ( Brinton et al, 2015 ), is also associated with rise in chronic low-grade inflammation ( Yin et al, 2015 ). Chronic systemic inflammation accelerates ovarian failure ( Ağaçayak et al, 2016 ). Conversely, depleting proinflammatory cytokines IL-1α and IL-1β extends ovarian function and lifespan ( Uri-Belapolsky et al, 2014 ).…”

Section: Menopause Inflammation and Admentioning

confidence: 99%

Inflammation: Bridging Age, Menopause and APOEε4 Genotype to Alzheimer’s Disease

Mishra

Brinton

2018

Front. Aging Neurosci.

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Neuro-inflammatory processes that contribute to development of Alzheimer’s are evident early in the latent prodromal phase and worsen during the course of the disease. Despite substantial mechanistic and clinical evidence of inflammation, therapeutic approaches targeting inflammation have failed to alter the course of the disease. Disparate results from epidemiological and clinical trials targeting inflammation, highlight the complexity of the inflammatory process. Herein we review the dynamics of the inflammatory process across aging, midlife endocrine transitions, and the APOEε4 genotype and their contribution to progression of Alzheimer’s disease (AD). We discuss the chronic inflammatory processes that are activated during midlife chronological and endocrine aging, which ultimately limit the clearance capacity of microglia and lead to immune senescence. Aging, menopause, and APOEε4 combine the three hits of a compromised bioenergetic system of menopause with the chronic low grade innate inflammation of aging with the APOEε4 dyslipidemia and adaptive immune response. The inflammatory immune response is the unifying factor that bridges across each of the risk factors for AD. Immune system regulators that are specific to stage of disease and inflammatory phenotype would provide a therapeutic strategy to disconnect the bridge that drives disease. Outcomes of this analysis provide plausible mechanisms underlying failed clinical trials of anti-inflammatory agents in Alzheimer’s patients. Further, they highlight the need for stratifying AD clinical trial cohorts based on inflammatory phenotype. Combination therapies that include targeted use of anti-inflammatory agent’s specific to the immune phenotype are considered.

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Role of inflammation and oxidative stress in the etiology of primary ovarian insufficiency

Cited by 34 publications

References 33 publications

Protective effects of mangafodipir against chemotherapy-induced ovarian damage in mice

Protective effects of mangafodipir against chemotherapy-induced ovarian damage in mice

Towards an understanding of women's brain aging: the immunology of pregnancy and menopause

Inflammation: Bridging Age, Menopause and APOEε4 Genotype to Alzheimer’s Disease

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