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Showing 6 results for Arun

Sayee Rajangam, Preetha Tilak, Aruna N, Rema Devi,
Volume 5, Issue 2 (7-2007)
Abstract

Background: Division of Human Genetics (DHG) is a referral center for karyotyping and counseling to the couples as well as to the individuals referred with bad obstetric history and infertility.
Materials and Methods: From 1972 to 2003, overall 1666 couples and 131 female partners with bad obstetric history (BOH) such as; spontaneous abortions, live births with congenital malformations and still born and 73 infertile male partners have been referred for chromosomal analysis.
Results: The chromosomal abnormality was found in 4.4% (83) of the sample studied. Chromosomal abnormality was seen in 56 couples (3.4%), 15 female (11.5%) and 12 male (16.4%) partners. The numerical chromosomal abnormality were seen in 34 (41%) and the structural abnormalities in 49 (59%) cases. The numerical chromosomal abnormalities were associated with sex chromosomes as follows (the number of cases are shown in parenthesis): 47, XXY (9); 46, XY/ 47, XXY (2); 46, XY/ 48, XXXY (1); 46, XY/ 47, XYY (2) and X mosaicism; 45, X/ 46, XX (14); 46, XX/ 47, XXX (6). The structural anomalies were 40 translocations and 9 duplication/ deletion/ marker/ iso chromosome for the X chromosome; Male: 46,XY/ 47,XY+ mar (1); Female: 45,X/ 47,XX+mar (1); 46,XX/ 47,XX+mar (1); 47,XX+frag (1); 46,X,Xq- (2); 46,X,Xp- (1); 46,X,Xp+ (1); 45,X/46,X,i(Xq)(1). The frequently involved chromosomes in the translocations were 4, 11, 15 and X. There were three X; autosomal translocations and a unique combination of translocation 1; 15 in the parents of a female carrier and 13; 14 in a non- consanguineous couple. On the whole, 57.5% of the females (23/ 40) were translocation carriers. Non-significant chromosome polymorphisms were observed in 79 cases (4.2%).
Conclusion: The current study has demonstrated the presence of the chromosomal abnormality and its influence in reproductive failure. On an average, in this study one in 56 couple and one in 12 males with infertility or one in 15 females with BOH has had a chromosomal abnormality as the genetic cause. The identification of chromosomal abnormality as the etiology has facilitated the counseling and appropriate management.
Supatcharee Arun, Jaturon Burawat, Wannisa Sukhorum, Apichakan Sampannang, Chanwit Maneenin, Sitthichai Iamsaard,
Volume 14, Issue 7 (7-2016)
Abstract

Background: Stress is a cause of male infertility. Although sex hormones and sperm quality have been shown to be low in stress, sperm physiology and testicular functional proteins, such as phosphotyrosine proteins, have not been documented. 
Objective: To investigate the acrosome status and alterations of testicular proteins involved in spermatogenesis and testosterone synthesis in chronic stress in rats. 
Materials and Methods: In this experimental study, male rats were divided into 2 groups (control and chronic stress (CS), n=7). CS rats were immobilized (4 hr/day) for 42 consecutive days. The blood glucose level (BGL), corticosterone, testosterone, acrosome status, and histopathology were examined. The expressions of testicular steroidogenic acute regulatory (StAR), cytochrome P450 side chain cleavage (CYP11A1), and phosphorylated proteins were analyzed. 
Results: Results showed that BGL (71.25±2.22 vs. 95.60±3.36 mg/dl), corticosterone level (24.33±4.23 vs. 36.9±2.01 ng/ml), acrosome reacted sperm (3.25±1.55 vs. 17.71±5.03%), and sperm head abnormality (3.29±0.71 vs. 6.21±1.18%) were significantly higher in CS group in comparison with control. In contrast, seminal vesicle (0.41±0.05 vs. 0.24±0.07 g/100g), testosterone level (3.37±0.79 vs. 0.61±0.29 ng/ml), and sperm concentration (115.33±7.70 vs. 79.13±3.65×106 cells/ml) of CS were significantly lower (p<0.05) than controls. Some atrophic seminiferous tubules and low sperm mass were apparent in CS rats. The expression of CYP11A1 except StAR protein was markedly decreased in CS rats. In contrast, a 55 kDa phosphorylated protein was higher in CS testes. 
Conclusion: CS decreased the expression of CYP11A, resulting in decreased testosterone, and increased acrosome-reacted sperm, assumed to be the result of an increase of 55 kDa phosphorylated protein.
Sitthichai Iamsaard, Wannisa Sukhorum, Supatcharee Arun, Nichapa Phunchago, Nongnuch Uabundit, Porntip Boonruangsri, Malivalaya Namking,
Volume 15, Issue 4 (6-2017)
Abstract

Background: Valproic acid (VPA), an anti-epileptic drug, can cause male subfertility. However, the degree to which testicular and epididymal histopathologies and androgen receptor (AR) expression are changed under VPA treatment has never been reported.
Objective: To investigate the histopathological changes and AR protein levels of testis and epididymis in VPA-treated rats for every single day.
Materials and Methods: Sixty-four adult male Wistar rats were divided intocontrol and VPA-treated groups (n=8/ each). Treated rats were injected with 500mg/ kgBW, intraperitoneally, VPA for 10 consecutive days. At the end of everyexperimental day, all reproductive parameters including histology by hematoxylinand eosin staining and protein expression of AR by Immuno-Western blot in testisand epididymis were examined.
Results: VPA-treated rats showed dramatically changes in testicular and epididymal histopathologies compared to control group. The multinucleated giant cells and sloughing of germ cells were observed on day 6. The germ cell disintegration and increased intercellular spaces of seminiferous tubular epithelium appeared in days 7-10 of VPA treatment. Additionally, extensive multinucleated giant cells and complete exfoliation were clearly found from days 8-10. Such exfoliated germ cells were clearly seen in its epididymal lumen at day 10. The increasing rate of sperm concentration was approximately 32.31% of that in control group at day 10 (p=0.03). Moreover, the protein expressions of testicular and epididymal AR (% intensity/ 80 μg protein lysate) was decreased in VPA-treated rats compared with control.
Conclusion: VPA treatment induces histologic changes of germ cell epithelium in seminiferous tubules and decreases the expression of testicular and epididymal
Apichakan Sampannang, Supatcharee Arun, Jaturon Burawat, Wannisa Sukhorum, Sitthichai Iamsaard,
Volume 16, Issue 4 (April 2018)
Abstract

Background: The streptozotocin (STZ)-induced diabetic model is widely used to evaluate the adverse effects of diabetes mellitus (DM) on spermatogenesis and testicular steroidogenesis. However, the actual mechanism of sub/infertility in DM males needs to be elucidated.
Objective: To conduct a detailed examination of the testicular histopathology, sperm acrosome reaction (AR) status, and tyrosine-phosphorylated protein expression in the testis of male mice induced with STZ.
Materials and Methods: Ten ICR mice were divided into two groups (n=5/each): control and diabetes induced by multiple low doses of streptozotocin (MLD-STZ). The control mice were intraperitoneally injected with citrate buffer, whereas MLD-STZ mice were injected with STZ at 40 mg/kg body weight for five consecutive days. At the end of the experiment (day 40), reproductive parameters, AR status, and the histopathology of the testis and epididymis were evaluated. The expression of testicular tyrosine phosphorylated proteins was examined.
Results: Blood glucose levels, AR percentages, and sperm abnormality of STZ group were significantly higher (p=0.003, 0.001, 0.000), while sperm concentration was significantly lower (p=0.001) compared to control. Histopathology of the seminiferous tubule was classified into 7 types. Additionally, abundant round cells were found in the epididymal lumen of the MLD-STZ mice. Moreover, the intensities of testicular phosphorylated proteins (170, 70, 36, 30, and 25 kDas) were markedly higher and a 120 kDa protein band was noticeably lower in the MLD-STZ mice.
Conclusion: MLD-STZ-induced DM causes many testicular histopathologies, precocious sperm AR, and increased expression of testicular phosphorylated proteins. These findings may clarify some mechanisms of sub/infertility in DM males.
Apichakan Sampannang, Supatcharee Arun, Jaturon Burawat, Wannisa Sukhorum, Sitthichai Iamsaard,
Volume 17, Issue 8 (August 2019)
Abstract

Background: Types 1 and 2 diabetes mellitus (DM) are known to be the cause of sub/infertility. However, the comparisons of potential markers in spermatogenesis and steroidogenesis in DM males have never been elucidated.
Objective: This study aimed to examine the expressions of tyrosine-phosphorylated and steroidogenic acute regulatory (StAR) proteins in testis of DM mice.
Materials and Methods: Fifty-six male C57BL/6 mice were divided into four groups (n = 14/ each): control of MLD-STZ (multiple low doses of streptozotocin), MLD-STZ, control of HFD-STZ (high-fat diet with STZ), and HFD-STZ. MLD-STZ mice (type 1 DM) were intraperitoneally (i.p.) injected with STZ at 40 mg/kg BW for five days. HFD-STZ mice (type 2 DM) received an HFD for 14 days and i.p.-induced by STZ at 85 mg/kg BW and fed with HFD. At the end of the experiment (days 36 and 72), the expressions of phosphorylated proteins and StAR were examined.
Results: Tyrosine phosphorylated proteins were localized in late spermatids, luminal fluid, and Leydig cells. The intensities of phosphorylated 110, 85, 72, 60, and 55 kDas were lower in the 36 day-DM mice. Although such intensities were present in both groups, only 85 kDa in the MLD-STZ mice was higher in HFD mice at 72 days. StAR expressions in both groups were decreased than that of the controls.
Conclusion: Decreased expressions of StAR and tyrosine-phosphorylated proteins may be directly involved in low testosterone levels and impaired spermatogenesis. These findings support the notion that both DM types play a role in male infertility.
Sudtida Bunsueb, Natthapol Lapyuneyong, Saranya Tongpan, Supatcharee Arun, Sitthichai Iamsaard,
Volume 19, Issue 1 (January 2021)
Abstract

Background: Changes in tyrosine-phosphorylated (TyrPho) protein expressions have demonstrated stress in males. In females, chronic stress (CS) is a major cause of infertility, especially anovulation. However, the tyrosine phosphorylation in the female reproductive system under stress conditions has never been reported.
Objective: To investigate the alteration of TyrPho protein expression in ovary, oviduct, and uterus of CS rats. 
Materials and Methods: In this experimental study, 16 female Sprague-Dawley rats (5 wk: 220-250 gr) were divided into control and CS groups (n = 8/group). Every day, the CS animals were immobilized within a restraint cage and individually forced to swim in cold water for 60 consecutive days. Following the stress induction, the ovary, oviduct, and uterus of all rats were observed for their morphologies. The total protein profiles of all tissues were revealed by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) before detecting TyrPho proteins using western blot. Intensity analysis was used to compare the expression of proteins between groups.
Results: The results showed that the morphology and weights of ovary and oviduct in the CS group were not different from control. In contrast, the CS significantly increased the uterine weight as compared to control. Moreover, the expressions of TyrPho proteins in the ovary (72, 43, and 28 kDas), oviduct (170, 55, and 43 kDas), and uterus (55, 54, and 43 kDas) were increased in CS group as compared to those of control.
Conclusion: The increased expressions of TyrPho proteins in ovary, oviduct, and uterus could be potential markers used to explain some machanisms of female infertility caused from chronic stress.
 


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