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      Light-exposure at night impairs mouse ovary development via cell apoptosis and DNA damage

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          Abstract

          The alternation of light and dark rhythm causes a series of physiological, biochemical and metabolic changes in animals, which also alters the growth and development of animals, and feeding, migration, reproduction and other behavioral activities. In recent years, many studies have reported the effects of long-term (more than 6 weeks) illumination on ovarian growth and development. In the present study, we observed the damage, repair and apoptosis of ovarian DNA in a short period of illumination. The results showed that, in short time (less than 2 weeks) illumination conditions, the 24-h light treatment caused the reduction of total ovarian follicle number and down-regulation of circadian clock related genes. Furthermore, the changed levels of serum sex hormones were also detected after 24-h light exposure, of which the concentrations of LH (luteinizing hormone), FSH (follicle-stimulating hormone) and E2 (estradiol) were increased, but the concentration of PROG (progesterone) was decreased. Moreover, 24-h light exposure increased the expression of DNA damage and repair related genes, the number of TUNEL and RAD51 positive cells. These results indicated that 24-h light exposure for 4, 8 and 12 days increased DNA damage and cell apoptosis, thereby affecting the development of ovary.

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          Most cited references61

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          Molecular architecture of the mammalian circadian clock.

          Circadian clocks coordinate physiology and behavior with the 24h solar day to provide temporal homeostasis with the external environment. The molecular clocks that drive these intrinsic rhythmic changes are based on interlocked transcription/translation feedback loops that integrate with diverse environmental and metabolic stimuli to generate internal 24h timing. In this review we highlight recent advances in our understanding of the core molecular clock and how it utilizes diverse transcriptional and post-transcriptional mechanisms to impart temporal control onto mammalian physiology. Understanding the way in which biological rhythms are generated throughout the body may provide avenues for temporally directed therapeutics to improve health and prevent disease. Copyright © 2013 Elsevier Ltd. All rights reserved.
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            Molecular components of the mammalian circadian clock.

            Circadian rhythms are approximately 24-h oscillations in behavior and physiology, which are internally generated and function to anticipate the environmental changes associated with the solar day. A conserved transcriptional-translational autoregulatory loop generates molecular oscillations of 'clock genes' at the cellular level. In mammals, the circadian system is organized in a hierarchical manner, in which a master pacemaker in the suprachiasmatic nucleus (SCN) regulates downstream oscillators in peripheral tissues. Recent findings have revealed that the clock is cell-autonomous and self-sustained not only in a central pacemaker, the SCN, but also in peripheral tissues and in dissociated cultured cells. It is becoming evident that specific contribution of each clock component and interactions among the components vary in a tissue-specific manner. Here, we review the general mechanisms of the circadian clockwork, describe recent findings that elucidate tissue-specific expression patterns of the clock genes and address the importance of circadian regulation in peripheral tissues for an organism's overall well-being.
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              Interacting molecular loops in the mammalian circadian clock.

              We show that, in the mouse, the core mechanism for the master circadian clock consists of interacting positive and negative transcription and translation feedback loops. Analysis of Clock/Clock mutant mice, homozygous Period2(Brdm1) mutants, and Cryptochrome-deficient mice reveals substantially altered Bmal1 rhythms, consistent with a dominant role of PERIOD2 in the positive regulation of the Bmal1 loop. In vitro analysis of CRYPTOCHROME inhibition of CLOCK: BMAL1-mediated transcription shows that the inhibition is through direct protein:protein interactions, independent of the PERIOD and TIMELESS proteins. PERIOD2 is a positive regulator of the Bmal1 loop, and CRYPTOCHROMES are the negative regulators of the Period and Cryptochrome cycles.
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                Author and article information

                Journal
                Biosci Rep
                Biosci. Rep
                ppbioscirep
                BSR
                Bioscience Reports
                Portland Press Ltd.
                0144-8463
                1573-4935
                08 April 2019
                31 May 2019
                02 May 2019
                : 39
                : 5
                : BSR20181464
                Affiliations
                [1 ]College of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266109, China
                [2 ]College of Life Sciences, Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, Qingdao Agricultural University, Qingdao 266109, China
                Author notes
                Correspondence: Xiaofeng Sun ( xfsun@ 123456qau.edu.cn )
                Author information
                http://orcid.org/0000-0003-3755-3269
                Article
                10.1042/BSR20181464
                6499499
                30962269
                7046382d-c97a-4da8-a067-7157e66aa7cc
                © 2019 The Author(s).

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                : 23 August 2018
                : 31 March 2019
                : 06 April 2019
                Page count
                Pages: 13
                Categories
                Research Articles
                Research Article
                32
                49
                13
                43
                55

                Life sciences
                apoptosis,clock related genes,dna damage,ovary,photoperiod
                Life sciences
                apoptosis, clock related genes, dna damage, ovary, photoperiod

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