Influence of Isoflurane Exposure for 15 Consecutive Days on Ovarian Function in Adult Female Mice

Tang, Xianan; Yao, Wen; Yao, Haijun; Zhang, Yi; Yue, Jing

doi:10.1007/s11596-020-2300-3

Cited by 3 publications

(3 citation statements)

References 24 publications

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“…At the same time, ROS can destroy a single or double strand of DNA and activate DNA-dependent protein kinases and P53, leading to cell apoptosis ( 37 ). Studies confirmed that NaF could improve HL-60 cells ( 109 ), testicular interstitial cells ( 110 ), H9C2 cardiomyopathy ( 111 ), oocytes ( 112 ), human lung BeAS-2B cells ( 113 ), rat liver and thymocytes ( 114 ), CytC, caspase-3, caspase-9 mid or protein levels are associated with apoptosis. After exposure to fluoride, the expression of caspase-3, caspase-9 and caspase-8 in fish kidney and porcine hepatocytes increased in a dose-dependent manner, indicating that fluoride can induce Caspase-dependent apoptosis.…”

Section: Potential Molecular Mechanism Of Mitochondrial Dysfunction I...mentioning

confidence: 86%

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Wei

Ali

et al. 2022

Front. Vet. Sci.

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Fluoride is commonly found in the soil and water environment and may act as chronic poison. A large amount of fluoride deposition causes serious harm to the ecological environment and human health. Mitochondrial dysfunction is a shared feature of fluorosis, and numerous studies reported this phenomenon in different model systems. More and more evidence shows that the functions of mitochondria play an extremely influential role in the organs and tissues after fluorosis. Fluoride invades into cells and mainly damages mitochondria, resulting in decreased activity of mitochondrial related enzymes, weakening of protein expression, damage of respiratory chain, excessive fission, disturbance of fusion, disorder of calcium regulation, resulting in the decrease of intracellular ATP and the accumulation of Reactive oxygen species. At the same time, the decrease of mitochondrial membrane potential leads to the release of Cyt c, causing a series of caspase cascade reactions and resulting in apoptosis. This article mainly reviews the mechanism of cytotoxicity related to mitochondrial dysfunction after fluorosis. A series of mitochondrial dysfunction caused by fluorosis, such as mitochondrial dynamics, mitochondrial Reactive oxygen species, mitochondrial fission, mitochondrial respiratory chain, mitochondrial autophagy apoptosis, mitochondrial fusion disturbance, mitochondrial calcium regulation are emphasized, and the mechanism of the effect of fluoride on cytotoxicity related to mitochondrial dysfunction are further explored.

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Section: Potential Molecular Mechanism Of Mitochondrial Dysfunction I...mentioning

confidence: 86%

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Wei

Ali

et al. 2022

Front. Vet. Sci.

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“…Although there exists a blood-follicle barrier in the ovary, it is not ironclad, and chemicals that can pass the germ cell barrier include lipid-soluble compounds and the PPARγ agonist rosiglitazone (Janesick & Blumberg, 2016 ). Studies have shown, for example, that anesthetic chemicals, which are lipid-soluble, are retained in follicular fluid following patient anesthesia (Christiaens et al, 1999 ), that excessive fluoride damaged oocytes in a mouse model (Wang et al, 2017 ), and that the halogenated anesthetic gas isoflurane resulted in a reduced number of developing follicles and an increased number of atretic follicles in mice (Tang et al, 2020 ). Around 300,000 oocytes remain at the start of puberty and there is a continued loss of about 1,000 follicles per month that accelerates with age, and reductions in the ovarian reserve are permanent, as female germ cells cannot be replaced (Orsi et al, 2014 ).…”

Section: A Primer On Vulnerabilities Of the Germ Cell Epigenome And G...mentioning

confidence: 99%

“…Anesthetic gases can cause significant DNA damage (Schifilliti et al, 2011 ), changes in gene expression, and epigenetic alterations (Martynyuk et al, 2020 ; Wang et al, 2021 ), in both exposed somatic and germ cells (Escher & Ford, 2020 ; Kaymak et al, 2012 ; Martynyuk et al, 2020 ; Wang et al, 2021 ). The damage caused by the gases also manifests in morphological and functional impairments in sperm (Coate et al, 1979 ; Land et al, 1981 ; Tang et al, 2020 ; Wang et al, 2008 ). The gases are also widely observed to act as steroid hormone disruptors, inducing dysfunction in the gonadal tissues and cells, with adverse impacts on germ cell integrity (Arena & Pereira, 2002 ; Kaya et al, 2013 ; Xu et al, 2012 ).…”

Section: Evidence Of Germ Cell Alterations Caused By Exogenous Factor...mentioning

confidence: 99%

Beyond Genes: Germline Disruption in the Etiology of Autism Spectrum Disorders

Escher¹,

Yan

Rissman

et al. 2021

J Autism Dev Disord

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Investigations into the etiology of autism spectrum disorders have been largely confined to two realms: variations in DNA sequence and somatic developmental exposures. Here we suggest a third route—disruption of the germline epigenome induced by exogenous toxicants during a parent’s gamete development. Similar to cases of germline mutation, these molecular perturbations may produce dysregulated transcription of brain-related genes during fetal and early development, resulting in abnormal neurobehavioral phenotypes in offspring. Many types of exposures may have these impacts, and here we discuss examples of anesthetic gases, tobacco components, synthetic steroids, and valproic acid. Alterations in parental germline could help explain some unsolved phenomena of autism, including increased prevalence, missing heritability, skewed sex ratio, and heterogeneity of neurobiology and behavior.

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How family histories can inform research about germ cell exposures: the example of autism

Escher¹

2021

Biology of Reproduction

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Throughout the scientific literature, heritable traits are routinely presumed to be genetic in origin. However, as emerging evidence from the realms of genetic toxicology and epigenomics demonstrate, heritability may be better understood as encompassing not only DNA sequence passed down through generations, but also disruptions to the parental germ cells causing de novo mutations or epigenetic alterations, with subsequent shifts in gene expression and functions in offspring. The Beyond Genes conference highlighted advances in understanding these aspects at molecular, experimental and epidemiological levels. In this commentary I suggest that future research on this topic could be inspired by collecting parents’ germ cell exposure histories, with particular attention to cases of families with multiple children suffering idiopathic disorders. In so doing I focus on the endpoint of autism spectrum disorders (ASD). Rates of this serious neurodevelopment disability have climbed around the world, a growing crisis that cannot be explained by diagnostic shifts. ASD’s strong heritability has prompted a research program largely focused on DNA sequencing to locate rare and common variants, but decades of this gene-focused research have revealed surprisingly little about the molecular origins of the disorder. Based on my experience as the mother of two children with idiopathic autism, and as a research philanthropist and autism advocate, I suggest ways researchers might probe parental germ cell exposure histories to develop new hypotheses that may ultimately reveal sources of non-genetic heritability in a subset of idiopathic heritable pathologies.

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Influence of Isoflurane Exposure for 15 Consecutive Days on Ovarian Function in Adult Female Mice

Cited by 3 publications

References 24 publications

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Beyond Genes: Germline Disruption in the Etiology of Autism Spectrum Disorders

How family histories can inform research about germ cell exposures: the example of autism

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