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    Morphological and biochemical investigation of the protective effects of panax ginseng on methotrexate-induced testicular damage
    (Istanbul University Press, 2023) Karakaya Çimen, Fatma Bedia; Macit, Çağlar; Sivas, Güzin Göksun; Tunalı Akbay, Tuğba; Şener, Göksel; Ercan, Feriha
    Objective: Methotrexate (MTX) is a chemotherapeutic agent that causes testicular toxicity used in the cure of various types of cancer. The anti-oxidant and anti-cancer effects of Panax ginseng (PxG) have been reported in both experimental and clinical studies. This study aims to examine the healing effect of PxG on testicular damage induced by MTX. Materials and Methods: Sprague Dawley male rats (8-week-olds) were used in the study. A single dose of MTX dissolved in saline (20 mg/kg) was given to MTX and MTX+PxG groups by intraperitoneal injection. PxG dissolved in saline (100 mg/kg) was given by orogastric gavage once a day for 5 days to the MTX+PxG group. Saline was given to the control and MTX groups orally during the experiments. After decapitation, the testis samples were obtained. Seminiferous tubules and basement membrane were evaluated histopathologically. Seminiferous tubule diameter and germinal epithelium thickness were measured. Furthermore, oxidative stress parameters such as malondialdehyde, glutathione, superoxide dismutase, and glutathione-S-transferase were measured. Results: MTX treatment caused seminiferous tubule degeneration with a decrease in Johnsen’s score, the seminiferous tubule’s diameter, and the germinal epithelium’s thickness. Parallel with the histopathological results increased testicular oxidative stress with an increase in malondialdehyde level and a decrease of endogenous anti-oxidant activity with a decrease in glutathione level and glutathione-S-transferase and superoxide dismutase activities. PxG treatment improved these histological and biochemical parameters in MTX-induced testis cytotoxicity. Conclusion: MTX treatment causes testicular damage via the oxidative processes. PxG treatment ameliorates MTX-induced testicular damage by inhibiting oxidative stress.
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    Panax ginseng extract ameliorates methotrexate-induced multi-organ damage via the regulation of oxidative stress
    (Marmara University, 2023) Macit, Çağlar; Ede Pazarbaşı, Seren; Yılmaz Karaoğlu, Sümeyye; Tunali Akbay, Tuğba; Karakaya Çimen, Fatma Bedia; Ercan, Feriha; Şener, Göksel
    Oxidative damage plays an important role in organ toxicities caused by methotrexate (MTX). This study aimed to determine the antioxidant effects of Panax ginseng (PxG) extract against MTX-induced liver, lung, ileum and kidney damage. Twenty-four Sprague Dawley male rats (weight 250-300 g) were used in the study. The animals were randomly separated into three groups: a) Control, b) MTX-treated (MTX) and c) MTX+PxG-treated (MTX+PxG) groups. MTX was administered intraperitoneally at 20 mg/kg, as a single dose to MTX and MTX+PxG groups. PxG was administered orally at 100 mg/kg to the MTX+PxG group for five days. Saline was given to the control and MTX groups for 5 days. At the end of the experiment, liver, lung, ileum, and kidney samples were obtained. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), glutathione-S-transferase (GST) and tissue factor (TF) activities were determined in all tissues. In addition, histological examinations were done through light microscopy. GraphPad Prism 5v. was used for statistics, and p[removed].
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    PPP2R3C gene variants cause syndromic 46,XY gonadal dysgenesis and impaired spermatogenesis in humans
    (Bioscientifica Ltd, 2019) Güran, Tülay; Yeşil, Gözde; Turan, Serap; Atay, Zeynep; Bozkurtlar, Emine; Aghayev, AghaRza; Gül, Sinem; Tinay, İlker; Aru, Başak; Arslan, Sema; Köroğlu, Mustafa Kutay; Ercan, Feriha; Yanıkkaya Demirel, Gülderen; Tanay Eren, Funda; Karademir, Betül; Bereket, Abdullah
    Context: Most of the knowledge on the factors involved in human sexual development stems from studies of rare cases with disorders of sex development. Here, we have described a novel 46, XY complete gonadal dysgenesis syndrome caused by homozygous variants in PPP2R3C gene. This gene encodes B '' gamma regulatory subunit of the protein phosphatase 2A (PP2A), which is a serine/threonine phosphatase involved in the phospho-regulation processes of most mammalian cell types. PPP2R3C gene is most abundantly expressed in testis in humans, while its function was hitherto unknown. Patients and methods: Four girls from four unrelated families with 46, XY complete gonadal dysgenesis were studied using exome or Sanger sequencing of PPP2R3C gene. In total, four patients and their heterozygous parents were investigated for clinical, laboratory, immunohistochemical and molecular characteristics. Results: We have identified three different homozygous PPP2R3C variants, c.308T>C (pL103P), c.578T>C (pL193S) and c.1049T>C (pF350S), in four girls with 46, XY complete gonadal dysgenesis. Patients also manifested a unique syndrome of extragonadal anomalies, including typical facial gestalt, low birth weight, myopathy, rod and cone dystrophy, anal atresia, omphalocele, sensorineural hearing loss, dry and scaly skin, skeletal abnormalities, renal agenesis and neuromotor delay. We have shown a decreased SOX9-Phospho protein expression in the dysgenetic gonads of the patients with homozygous PPP2R3C variants suggesting impaired SOX9 signaling in the pathogenesis of gonadal dysgenesis. Heterozygous males presented with abnormal sperm morphology and impaired fertility. Conclusion: Our findings suggest that PPP2R3C protein is involved in the ontogeny of multiple organs, especially critical for testis development and spermatogenesis. PPPR3C provides insight into pathophysiology, as well as emerging as a potential therapeutic target for male infertility.