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    Alpha-lipoic acid may ameliorate testicular damage by targeting dox-induced altered antioxidant parameters, mitofusin-2 and apoptotic gene expression
    (Andrologia, 2021) Güzel, Elif Erdem; Kaya Tektemur, Nalan; Tektemur, Ahmet
    In the study, the ameliorating effects of alfa lipoic acid (ALA) against doxorubicin-induced testicular apoptosis, oxidative stress and disrupted mitochondrial fusion were investigated in male rats. Rats were divided into four groups as control, doxorubicin (DOX), DOX + ALA and ALA. A single dose of 15 mg/kg DOX was administered i.p to the DOX and DOX + ALA groups. 50 mg/kg ALA was given to the DOX + ALA and ALA groups by oral gavage every other day. After 28 days, rat testes and serum samples were collected and analysed. Administration of DOX alone caused a decrease in body and relative testicular weights, seminiferous tubule diameter and germinal epithelium thickness, Johnsen's score and serum testosterone levels. DOX treatment led to severe testicular damage such as tubular degeneration, and atrophic tubules. Also, the activities of superoxide dismutase and glutathione peroxidase were reduced, while the level of malondialdehyde was increased in the testis. The mRNA levels of apoptotic-related genes (CASP3, TP53, BAX, BCL2) and apoptotic index were increased, while mitofusin-2 decreased. DOX caused an increase in CASP3 and a decrease in mitofusin-2 immunoreactivities. Treatment with ALA markedly improved all of DOX-induced biochemical, histochemical and molecular alterations in rat testis. Consequently, ALA has a therapeutic role in ameliorating DOX-induced testicular damage in rats.
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    The antioxidant and anti-apoptotic potential of Pleurotus eryngii extract and its chitosan-loaded nanoparticles against doxorubicin-induced testicular toxicity in male rats
    (Wiley, 2021) Erdem Güzel, Elif; Kaya Tektemur, Nalan; Tektemur, Ahmet; Acay, Hilal; Yıldırım, Ayfer
    This study was conducted to evaluate the protective role of Pleurotus eryngii extract (PE) and Pleurotus eryngii extract-loaded chitosan nanoparticles (PE-CSNP) against doxorubicin (DOX)-induced testicular toxicity in rats. Male rats were divided into six groups: control (DMSO/ethanol), PE (200 mg/kg PE), PE-CSNP (30 mg/kg PECSNP), DOX (10 mg/kg DOX, a single dose, i.p), DOX+PE (10 mg/kg DOX+200 mg/ kg PE) and DOX+PE-CSNP (10 mg/kg DOX+30 mg/kg PE-CSNP). PE and PE-CSNP were administered by oral gavage every other day for 21 days. DOX-treated rats showed histopathological impairment compared with the control group. There was an increase in the apoptotic index, caspase 3 (CASP3), BCL2-associated X apoptosis regulator (BAX), dynamin-related protein 1 (DRP1) expression and total oxidative status (TOS) in the DOX group, while mitofusin-2 (MFN2), total antioxidative status (TAS) and serum testosterone levels of the DOX group reduced when compared with the other groups. PE and PE-CSNP treatments provided significant protection against DOX-induced oxidative stress by reducing TOS levels and increasing TAS levels. CASP3, BAX, apoptotic index and DRP1-MFN2 expressions were restored by PE and PE-CSNP. However, the PE-CSNP showed higher antioxidant and anti-apoptotic efficacy compared with PE. Thus, our results provide evidence that CSNP and PE could synergistically have a potent antioxidant and anti-apoptotic therapy against DOX-induced testicular damage in male rats.
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    Carbamazepine-induced renal toxicity may be associated with oxidative stress and apoptosis in male rat
    (Taylor & Francis Online, 2021) Erdem Güzel, Elif; Kaya Tektemur, Nalan; Tektemur, Ahmet; Etem Önalan, Ebru
    Carbamazepine (CBZ) is the antiepileptic drug used in epilepsy and some psychiatric disorders. Besides its widely used, many adverse effects have been reported including hematotoxicity, hepatotoxicity, endocrine disorders, and testicular damages due to oxidative stress. However, the role of CBZ on renal toxicity is not fully known. In this study, we attempted to explain the connected mechanisms by focusing on the metabolism of CBZ-induced renal toxicity in rats. Twenty male Wistar-Albino rats were randomized into 2 groups (n = 10); control (1 mL/day distilled water, orally) and CBZ (25 mg/kg/day CBZ, orally) groups. After 60 days, TAS (total oxidant status) and TOS (total oxidant status) levels, histopathological features, some genes involved in apoptosis, 8-hydroxy-2-deoxyguanosine (8-OHdG) activity, and apoptotic cells were assessed of kidney tissue. The oxidative stress index (OSI) was measured from TAS and TOS levels. TOS levels and OSI significantly increased, while TAS levels decreased in the CBZ group relative to the control group. Histopathological observations, Caspase-3 (Casp3), Poly [ADP-ribose] polymerase-1 (PARP-1), 8-OHdG immunoreactivities, and apoptotic cells markedly raised in the CBZ group compared with the control group. Also, mRNA expression of Cytochrome c (Cytc) and CASP3 significantly increased in the CBZ group compared to the control group. In conclusion, long-term use of CBZ may promote renal damage in rats by inducing oxidative stress and apoptosis.
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    The combination of N-acetylcysteine and cyclosporin A reduces acetaminophen-induced hepatotoxicity in mice
    (Ultrastructural Pathology, 2021) Erdem Güzel, Elif; Kaya Tektemur, Nalan; Gül, Mehmet; Tektemur; Özcan Yıldırım, Sena; Kavak Balgetir, Merve; Ozan Kocamüftüoğlu, Gonca; Yalçın, Tuba; Ozan, & İbrahim Enver
    Acetaminophen (APAP)-induced hepatotoxicity is the most common cause of acute liver failure in worldwide. N-acetyl cysteine (NAC) is used as the APAP antidote. Cyclosporin A (CsA) is suppressed mitochondrial damage by binding cyclophilin, a mitochondrial pore transport component. The study aimed to evaluate the effects of NAC, CsA, and NAC+CsA treatments on APAP-induced hepatotoxicity in mice. Mice were randomly divided into five groups (n = 6). 400 mg/kg/ip/single dose APAP, 1200 mg/kg/i.p/single dose NAC and 50 mg/kg/i.p/single dose CsA were performed. Light and electron microscopic alterations were investigated in liver samples. Levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and liver glutathione (GSH) were analyzed. 3-nitrotyrosine and cytochrome c immunoreactivities were evaluated in liver tissue. Here, we found that APAP leads to histopathological and ultrastructural changes in mice liver. Also, APAP increased cytochrome c and 3-nitrotyrosine immunopositive staining. Besides, a significant decrease in liver GSH and an increase in serum AST and ALT levels were detected in the APAP group. Interestingly, NAC+CsA treatment improved histological alterations, cytochrome c, and 3-nitrotyrosine immunoreactivities and liver GSH, serum AST/ALT levels caused by APAP. We suggest that the combination of NAC and CsA reduces acetaminophen-induced hepatotoxicity in mice.
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    Hesperetin may alleviate the development of doxorubicin-induced pulmonary toxicity by decreasing oxidative stress and apoptosis in male rats
    (Elsevier, 2021) Erdem Güzel, Elif; Kaya Tektemur, Nalan
    Doxorubicin (DOX) is one of the most widely used chemotherapeutic agents. However, it causes pulmonary toxicity which decreases its clinical use in human cancer therapy. The present study was undertaken to obtain an insight into the potential protective effect of hesperetin (HES) against doxorubicin-induced pulmonary toxicity in rats. The animals were divided into 4 groups with 7 rats per group. The experimental treatments were as follows: Control, DOX, DOX + HES, and HES groups. DOX was administered at the dosage of 15 mg/kg i.p for a single dose. HES was administered at the dosage of 50 mg/kg by oral gavage every other day. After 28 days, biochemical parameters, oxidative stress status, histopathological changes, apoptosis-related genes and apoptotic index (AI) were examined of lung tissue. Histopathological changes, Poly [ADP-ribose] polymerase 1 (PARP-1), Caspase-3 (Casp3), Cytochrome c (Cytc), apoptosis-related genes, and AI significantly increased in the DOX group relative to the control group. Malondialdehyde (MDA) significantly increased, while superoxide dismutase (SOD) and glutathione peroxidase (GPx) decreased in the DOX group relative to the control group. However, histopathological findings, MDA, AI, and PAPR1, Casp3 protein expression, mRNA expression of Cytc significantly decreased, while SOD, GPx increased in the DOX + HES group relative to the DOX group. These results attested HES might be a potential agent for the treatment of DOX-induced pulmonary toxicity.
  • Küçük Resim Yok
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    King Oyster Mushroom, Pleurotus eryngii (Agaricomycetes), Extract Can Attenuate Doxorubicin-Induced Lung Damage by Inhibiting Oxidative Stress in Rats
    (International Journal of Medicinal Mushrooms, 2023) Kaya Tektemur, Nalan; Tektemur, Ahmet; Güzel, Elif Erdem
    Doxorubicin (DOX), a broad spectrum chemotherapeutic, has toxic effects on healthy tissues. Mitochondrial processes and oxidative stress act in the DOX-induced toxicity, therefore antioxidant therapies are widely used. The study was aimed to evaluate the therapeutic potential of Pleurotus eryngii extract (PEE), an extract of a fungus with antioxidant properties, against DOX-induced lung damage. Rats were divided into Control, DOX, DOX + PEE, and PEE groups (n = 6). DOX was administered intraperitoneally in a single dose (10 mg/kg BW) and PE (200 mg/kg BW) was administered by oral gavage every other day for 21 days. Histopathological evaluations, immunohistochemical analyses, total oxidant status (TOS)/total antioxidant status (TAS) method, and quantitative real-time polymerase chain reaction (qRT-PCR) analysis were performed. DOX led to severe histopathological disruptions in rat lungs. Also, DOX remarkably increased the expression of dynamin 1 like (DRP1) and decreased the expression of mitofusin 1 (MFN1) and mitofusin 2 (MFN2) genes, which are related to mitochondrial dynamics. Moreover, DOX caused an increase in TOS/ TAS and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels. On the other hand, PEE treatment remarkably normalized the histopathological findings, mitochondrial dynamics-related gene expressions, markers of oxidative stress, and DNA damage. The present study signs out that PEE can ameliorate the DOX-mediated lung toxicity and the antioxidant mechanism associated with mitochondrial dynamics can have a role in this potent therapeutic effect.
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    Pleurotus Eryngii Ekstraktının Sprague-Dawley Sıçanlarında Adriamisin Kaynaklı Kardiyotoksisite Üzerindeki Etkilerinin İncelenmesi
    (Dicle Tıp Dergisi, 2021) Erdem Güzel, Elif; Kaya Tektemur, Nalan; Tektemur, Ahmet; Acay, Hilal; Yıldırım, Ayfer
    Amaç: Adriamisin (ADR), kanser tedavilerinde kullanılan güçlü ve geniş spektrumlu bir antibiyotiktir. Fakat ADR’nin klinik etkinliği, doza bağlı kardiyotoksisitesi nedeniyle engellenmektedir. Bu nedenle çalışmada ADR uygulanan sıçanların kalp dokularında meydana gelen değişiklikler üzerine Pleurotus eryngii ekstraktının (PEE)’nin koruyucu etkisinin incelenmesi amaçlanmıştır. Yöntemler: Sprague-Dawley cinsi erkek sıçanlar 4 eşit gruba ayrıldı (n=6). Kontrol grubuna DMSO/etanol çözeltisi oral gavaj yolu ile gün aşırı verildi. ADR grubuna 10 mg/kg ADR intraperitoneal (i.p) olarak tek doz uygulandı. ADR+PEE grubuna 10 mg/kg i.p tek doz ADR verildikten sonra DMSO/etanol içinde çözdürülen 200 mg/kg PEE oral gavaj yoluyla gün aşırı verildi. PEE grubuna oral gavaj ile DMSO/etanolde çözdürülen 200 mg/kg PEE gün aşırı verildi. 21.günün sonunda sıçanlar dekapite edildi. Dekapitasyonun ardından kalp dokuları çıkarılarak histolojik ve kantitatif RT-PCR analizleri yapıldı. Bulgular: ADR grubuna ait kalp dokularında inflamatuar hücre artışı, miyofibril kaybı, sitoplazmik vakuolizasyon ve vasküler konjesyon bulgularına rastlanıldı. PEE tedavisinin bu histopatolojik bulgularda iyileşmeye neden olduğu gözlendi. Ayrıca ADR grubunda kontrol grubuna kıyasla IL1-β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir artış olduğu izlendi. ADR+PEE grubunda ise ADR grubuna kıyasla IL-1β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.Dekapitasyonun ardından kalp dokuları çıkarılarak histolojik ve kantitatif RT-PCR analizleri yapıldı. Bulgular: ADR grubuna ait kalp dokularında inflamatuar hücre artışı, miyofibril kaybı, sitoplazmik vakuolizasyon ve vasküler konjesyon bulgularına rastlanıldı. PEE tedavisinin bu histopatolojik bulgularda iyileşmeye neden olduğu gözlendi. Ayrıca ADR grubunda kontrol grubuna kıyasla IL1-β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir artış olduğu izlendi. ADR+PEE grubunda ise ADR grubuna kıyasla IL-1β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.Dekapitasyonun ardından kalp dokuları çıkarılarak histolojik ve kantitatif RT-PCR analizleri yapıldı. Bulgular: ADR grubuna ait kalp dokularında inflamatuar hücre artışı, miyofibril kaybı, sitoplazmik vakuolizasyon ve vasküler konjesyon bulgularına rastlanıldı. PEE tedavisinin bu histopatolojik bulgularda iyileşmeye neden olduğu gözlendi. Ayrıca ADR grubunda kontrol grubuna kıyasla IL1-β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir artış olduğu izlendi. ADR+PEE grubunda ise ADR grubuna kıyasla IL-1β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.ADR grubuna ait kalp dokularında inflamatuar hücre artışı, miyofibril kaybı, sitoplazmik vakuolizasyon ve vasküler konjesyon bulgularına rastlanıldı. PEE tedavisinin bu histopatolojik bulgularda iyileşmeye neden olduğu gözlendi. Ayrıca ADR grubunda kontrol grubuna kıyasla IL1-β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir artış olduğu izlendi. ADR+PEE grubunda ise ADR grubuna kıyasla IL-1β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.ADR grubuna ait kalp dokularında inflamatuar hücre artışı, miyofibril kaybı, sitoplazmik vakuolizasyon ve vasküler konjesyon bulgularına rastlanıldı. PEE tedavisinin bu histopatolojik bulgularda iyileşmeye neden olduğu gözlendi. Ayrıca ADR grubunda kontrol grubuna kıyasla IL1-β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir artış olduğu izlendi. ADR+PEE grubunda ise ADR grubuna kıyasla IL-1β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.PEE tedavisinin bu histopatolojik bulgularda iyileşmeye neden olduğu gözlendi. Ayrıca ADR grubunda kontrol grubuna kıyasla IL1-β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir artış olduğu izlendi. ADR+PEE grubunda ise ADR grubuna kıyasla IL-1β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.PEE tedavisinin bu histopatolojik bulgularda iyileşmeye neden olduğu gözlendi. Ayrıca ADR grubunda kontrol grubuna kıyasla IL1-β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir artış olduğu izlendi. ADR+PEE grubunda ise ADR grubuna kıyasla IL-1β immunoreaktivitesinde ve IL1-β, BAX, Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.Kaspaz-3 mRNA seviyelerinde anlamlı bir azalma olduğu belirlendi. Sonuç: ADR’ye bağlı kardiyotoksisitede PEE tedavisinin anti-apoptotik ve anti-inflamatuar özellikleri ile kardiyoprotektif etki gösterdiği ortaya koyuldu.
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    The therapeutic effect of hesperetin on doxorubicin-induced testicular toxicity: Potential roles of the mechanistic target of rapamycin kinase (mTOR) and dynamin-related protein 1 (DRP1)
    (Elsevier, 2022) Tektemur, Ahmet; Kaya Tektemur, Nalan; Erdem Güzel, Elif
    Clinical utilization of doxorubicin (DOX), which is a commonly used chemotherapeutic, is restricted due to toxic effects on various tissues. Using hesperetin (HST), an antioxidant used in Chinese traditional medicine protects testis against DOX-induced toxicity although the molecular mechanisms are not well-known. The study was aimed to examine the possible role of the mechanistic target of rapamycin kinase (mTOR) and dynamin 1-like dynamin-related protein 1 (DRP1) in the therapeutic effects of HST on the DOX-induced testicular toxicity. Rats were divided into Control, DOX, DOX + HST, and HST groups (n = 7). Single-dose DOX (15 mg/kg) was administered intraperitoneally and HST (50 mg/kg) was administered by oral gavage every other day for 28 days. Total antioxidant status (TAS), histopathological evaluations, immunohistochemistry, and gene expression level detection analyses were performed. Histopathologically, DOX-induced testicular damage was ameliorated by HST treatment. DOX reduced testicular TAS levels and increased oxidative stress markers, 8-Hydroxy-deoxyguanosine (8-OHdG), and 4-Hydroxynonenal (4-HNE). Also, upregulated mTOR and DRP1 expressions with DOX exposure were decreased after HST treatment in the testis (p < 0.05). On the other hand, DOX-administration downregulated miR-150-5p and miR-181b-2-3p miRNAs, targeting mTOR and mRNA levels of beclin 1 (BECN1) and autophagy-related 5 (ATG5), autophagic markers. Furthermore, these levels were nearly similar to control testis samples in the DOX + HST group (p < 0.05). The study demonstrated that HST may have a therapeutic effect on DOX-induced testicular toxicity by removing reactive oxygen species (ROS) and by modulating the mTOR and DRP1 expressions, which have a critical role in regulating the balance of generation/elimination of ROS.