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      Effect of noise stress on count, progressive and non-progressive sperm motility, body and genital organ weights of adult male rats


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          It was decided to investigate the effect of noise pollution on the body weight, genital organ weights, and also on sperm parameters.


          It is a prospective study designed in vitro.


          A total 20 adult male wistar rats were used in this study. All rats were divided into 2 equal groups ( n = 10): (1) control group and (2) experimental group. Animals of the experimental group were exposed to noise for 50 days with an intensity of 90-120 db and frequency of 300 - 350 Hz for 12 hours daily. After 50 days, at first, body weights of all animals were recorded, and then they were killed. The right epididymides were removed and also, sperm concentration and motility were determined. Each organ was weighed separately on an electronic balance.


          Data are reported as mean ± SD and percentage. The statistical significance of difference between the control and experimental groups was determined by the unpaired t-test.


          The weights of the testes, epididymes, seminal vesicle, ventral prostate were found to be significantly decreased in rats exposed to noise pollution when compared with the weights of the same organs obtained from control group ( P < 0.05). There was a statistical difference of P < 0.05 between the 2 groups in terms of sperm concentration.


          It is concluded that noise pollution has the bad effects on sperm concentration and motility; therefore, it is supposed that homes and places of working must be build far away of noisy of factories and other places with noise.

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          Most cited references26

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          Effects of heat stress on mammalian reproduction.

          Heat stress can have large effects on most aspects of reproductive function in mammals. These include disruptions in spermatogenesis and oocyte development, oocyte maturation, early embryonic development, foetal and placental growth and lactation. These deleterious effects of heat stress are the result of either the hyperthermia associated with heat stress or the physiological adjustments made by the heat-stressed animal to regulate body temperature. Many effects of elevated temperature on gametes and the early embryo involve increased production of reactive oxygen species. Genetic adaptation to heat stress is possible both with respect to regulation of body temperature and cellular resistance to elevated temperature.
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            Stress hormones in the research on cardiovascular effects of noise.

            W Babisch (2015)
            In recent years, the measurement of stress hormones including adrenaline, noradrenaline and cortisol has been widely used to study the possible increase in cardiovascular risk of noise exposed subjects. Since endocrine changes manifesting in physiological disorders come first in the chain of cause-effect for perceived noise stress, noise effects in stress hormones may therefore be detected in populations after relatively short periods of noise exposure. This makes stress hormones a useful stress indicator, but regarding a risk assessment, the interpretation of endocrine noise effects is often a qualitative one rather than a quantitative one. Stress hormones can be used in noise studies to study mechanisms of physiological reactions to noise and to identify vulnerable groups. A review is given about findings in stress hormones from laboratory, occupational and environmental studies.
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              Fetal testosterone insufficiency and abnormal proliferation of Leydig cells and gonocytes in rats exposed to di(n-butyl) phthalate.

              Adult male rats previously exposed on gestation days (GD) 12-21 to di(n-butyl) phthalate (DBP) have reproductive tract malformations, particularly agenesis of the epididymis, decreased sperm production, and Leydig cell hyperplasia and adenomas. Although similar effects are produced by the potent androgen receptor (AR) antagonist flutamide and are indicative of disruption of male sexual differentiation via an antiandrogenic mechanism, DBP is not an AR antagonist. The purpose of the study was to determine whether DBP causes pathologic changes and alterations in androgen status in the testis during the prenatal period of male reproductive tract differentiation. Pregnant CD rats were given corn oil, DBP (500 mg/kg/day), or flutamide (100 mg/kg/day) p.o. on GD 12-21. At GD 16-21, DBP caused hyperplasia of Leydig cells, many of which were 3beta-hydroxysteroid dehydrogenase- and/or AR-positive. Focal areas of hyperplasia had increased numbers of Leydig cells positive for proliferating cell nuclear antigen (PCNA). At GD 21, testis atrophy was apparent, seminiferous cords in DBP-exposed fetuses were enlarged and contained multinucleated gonocytes that, unlike controls, were PCNA-positive. DBP, but not flutamide, markedly decreased testicular testosterone levels at GD 18 and 21. Fewer epididymal ducts and reduced AR staining in some ducts were evident with DBP treatment, whereas decreased overall AR staining was seen with flutamide in the presence of mild Leydig cell hyperplasia. Leydig cell proliferation is likely a compensatory mechanism to increase testicular steroidogenesis triggered by testosterone insufficiency. The overall decrease in androgen concentration is not corrected and results in reproductive tract malformations. The multinuclearity and proliferation of gonocytes suggests an underlying Sertoli cell dysfunction.

                Author and article information

                J Hum Reprod Sci
                J Hum Reprod Sci
                Journal of Human Reproductive Sciences
                Medknow Publications & Media Pvt Ltd (India )
                Jan-Apr 2012
                : 5
                : 1
                : 48-51
                [1]Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
                [1 ]Department of Biology, Payamenour University, Tehran, Iran
                Author notes
                Address for correspondence: Mr. Ghasem Saki, Department of Anatomical Science, Faculty of Medicine, Ahvaz Joundishapour University of Medical Science, Ahvaz, Iran. E-mail: ghasemsaki@ 123456yahoo.com
                Copyright: © Journal of Human Reproductive Sciences

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Original Article

                Human biology
                Human biology
                pregnancy, infertility, hormone, pollution


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