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15. Protective Effects of Syringic Acid Against Oxidative Damage, Apoptosis, Autophagy, Inflammation, Testicular Histopathologic Disorders, and Impaired Sperm Quality in the Testicular Tissue of Rats Induced by Mercuric Chloride.

Author

Akarsu, Serkan Ali, Gür, Cihan, Küçükler, Sefa, Akaras, Nurhan, İleritürk, Mustafa, and Kandemir, Fatih Mehmet

Subjects
SYRINGIC acid, ORAL drug administration, MERCURIC chloride, BIOLOGICAL membranes, HEAVY metals, ENDOPLASMIC reticulum
Abstract

Mercury (Hg) is one of the most toxic heavy metals that damage testicular tissue. Mercury chloride (HgCl2) is one of the most toxic forms of mercury that can easily cross biological membranes. Syringic acid (SA) is a natural flavonoid found in many vegetables and fruits. In this study, the effects of SA against HgCl2‐induced testicular damage in rats were determined by biochemical, histopathological, and spermatological analyses. For this study, a total of 35 Spraque Dawley rats were used. Rats were divided into five groups as control, HgCl2, SA 50, HgCl2 + SA 25, and HgCl2 + SA 50. HgCl2 was administered intraperitoneal (IP) at a dose of 1.23 mg/kg/bw, while SA was administered by oral gavage at doses of 25 and 50 mg/kg/bw. The rats were then sacrificed, and testicular tissues were removed. HgCl2 caused an increase in MDA level and a decrease in SOD, CAT, and GPx activity and GSH level in the testicular tissue of rats. HgCl2 is involved in the increase of eIF2‐α, PERK, ATF‐4, ATF‐6, CHOP, NF‐κB, TNF‐α, IL‐1β, Apaf‐1, Bax, and Caspase‐3 mRNA expression. HgCl2 caused a decrease in sperm motility, an increase in the rate of abnormal sperm and sperm DNA fragmentation in rats. However, SA oral administration dose‐dependently inhibited endoplasmic reticulum stress, oxidative stress, inflammation, and apoptosis and preserved epididymal sperm quality and testicular histoarchitectures. In conclusion, SA had protective effects against HgCl2‐induced testicular oxidative damage, inflammation, endoplasmic reticulum stress, and apoptosis. [ABSTRACT FROM AUTHOR]

Published
2024
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16. The ameliorative effect of carvacrol on sodium arsenite‐induced hepatotoxicity in rats: Possible role of Nrf2/HO‐1, RAGE/NLRP3, Bax/Bcl‐2/Caspase‐3, and Beclin‐1 pathways.

Author

Gencer, Selman, Gür, Cihan, İleritürk, Mustafa, Küçükler, Sefa, Akaras, Nurhan, Şimşek, Hasan, and Kandemir, Fatih M.

Subjects
POLLUTANTS, GLUTATHIONE peroxidase, CARVACROL, HEPATOTOXICOLOGY, SODIUM arsenite
Abstract

Arsenic is a toxic environmental pollutant heavy metal, and one of its critical target tissues in the body is the liver. Carvacrol is a natural phytocompound that stands out with its antioxidant, anti‐inflammatory, and antiapoptotic properties. The current study aims to investigate the protective feature of carvacrol against sodium arsenite‐induced liver toxicity. Thirty‐five Sprague‐Dawley male rats were divided into five groups: Control, Sodium arsenite (SA), CRV, SA + CRV25, and SA + CRV50. Sodium arsenite was administered via oral gavage at a dose of 10 mg/kg for 14 days, and 30 min later, CRV 25 or 50 mg/kg was administered via oral gavage. Oxidative stress, inflammation, apoptosis, autophagy damage pathways parameters, and liver tissue integrity were analyzed using biochemical, molecular, western blot, histological, and immunohistological methods. Carvacrol decreased sodium arsenite‐induced oxidative stress by suppressing malondialdehyde levels and increasing superoxide dismutase, catalase, glutathione peroxidase activities, and glutathione levels. Carvacrol reduced inflammation damage by reducing sodium arsenite‐induced increased levels of NF‐κB and the cytokines (TNF‐α, IL‐1β, IL‐6, RAGE, and NLRP3) it stimulates. Carvacrol also reduced sodium arsenite‐induced autophagic (Beclin‐1, LC3A, and LC3B) and apoptotic (P53, Apaf‐1, Casp‐3, Casp‐6, Casp‐9, and Bax) parameters. Carvacrol preserved sodium arsenite‐induced impaired liver tissue structure. Carvacrol alleviated toxic damage by reducing sodium arsenite‐induced increases in oxidative stress, inflammation, apoptosis, and autophagic damage parameters in rat liver tissues. Carvacrol was also beneficial in preserving liver tissue integrity. [ABSTRACT FROM AUTHOR]

Published
2024
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19. Kurşun Kaynaklı Oluşan Dalak Toksisitesine Karşı Sinapik Asidin Etkilerinin İncelenmesi.

Author

DALKILINÇ, Elif, KÜÇÜKLER, Sefa, and AYDIN, Şeyma

Subjects
SUPEROXIDE dismutase, GLUTATHIONE peroxidase, SPLEEN, LEAD, ORAL drug administration
Abstract

Copyright of Journal of Laboratory Animal Science & Practices / Laboratuvar Hayvanlari Bilimi ve Uygulamalari Dergisi is the property of Ataturk University Coordinatorship of Scientific Journals and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2024
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20. Naringin protects against paclitaxel‐induced toxicity in rat testicular tissues by regulating genes in pro‐inflammatory cytokines, oxidative stress, apoptosis, and JNK/MAPK signaling pathways.

Author

Kankılıç, Nazım Abdülkadir, Küçükler, Sefa, Gür, Cihan, Akarsu, Serkan Ali, Akaras, Nurhan, Şimşek, Hasan, İleritürk, Mustafa, and Kandemir, Fatih Mehmet

Subjects
PACLITAXEL, OXIDATIVE stress, NF-kappa B, NARINGIN, TUMOR necrosis factors, CELL death, MITOGEN-activated protein kinases, MYELOID differentiation factor 88
Abstract

Paclitaxel (PTX), which is actively used in the treatment of many types of cancer, has a toxic effect by causing increased oxidative stress in testicular tissues. Naringin (NRG) is a natural flavonoid found in plants, and its antioxidant properties are at the forefront. This study aims to investigate the protective feature of NRG in PTX‐induced testicular toxicity. Thirty‐five male Sprague rats were divided into five groups: control, NRG, PTX, PTX + NRG50, and PTX + NRG100. Rats were administered PTX (2 mg/kg, BW) intraperitoneally once daily for the first 5 days. Then, between the 6th and 14th days, NRG (50 and 100 mg/kg) was administered orally once a day. NRG reduced PTX‐induced lipid peroxidation and increased testicular tissue antioxidant capacity (superoxide dismutase, catalase, glutathione peroxidase, and glutathione). While NRG reduces the mRNA expression levels of nuclear factor kappa B, tumor necrosis factor‐alpha, interleukin‐1 beta, cyclooxygenase‐2, interleukin‐6, inducible‐nitric oxide synthase, mitogen‐activated protein kinase 14 (MAPK)14, MAPK15, c‐Jun N‐terminal kinase, P53, Apaf1, Caspase3, Caspase6, Caspase9, and Bax in testicular tissues; it caused an increase in Nrf2, HO‐1, NQO1 and Bcl‐2 levels. NRG also improved the structural and functional integrity of testicular tissue disrupted by PTX. PTX‐induced sperm damage was alleviated by NRG. NRG showed a protective effect by alleviating the PTX‐induced testicular toxicity by increasing oxidative stress, inflammation, apoptosis, and autophagy. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Protective effects of naringin on colistin‐induced damage in rat testicular tissue: Modulating the levels of Nrf‐2/HO‐1, AKT‐2/FOXO1A, Bax/Bcl2/Caspase‐3, and Beclin‐1/LC3A/LC3B signaling pathways

Author

Kankılıç, Nazım Abdülkadir, primary, Şimşek, Hasan, additional, Akaras, Nurhan, additional, Gür, Cihan, additional, İleritürk, Mustafa, additional, Küçükler, Sefa, additional, Akarsu, Serkan A., additional, and Kandemir, Fatih M., additional

Published
2024
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24. E. coli ve Rotavirusların Neden Olduğu Neonatal Dönem Buzağı İshallerinde Klinik, Hematolojik ve IL-8 Düzeyi Üzerine Bir Araştırma.

Author

EROĞLU, Muhammed Sertaç, HANEDAN, Başak, EREN, Emre, KÜÇÜKLER, Sefa, and AKTAŞ, Mustafa Sinan

Subjects
RAPID diagnostic tests, ESCHERICHIA coli, VIRAL diarrhea, JUGULAR vein, DIAGNOSTIC reagents & test kits
Abstract

Copyright of Firat Universitesi Saglik Bilimleri Veteriner Dergisi is the property of Firat Universitesiu, Saglik Bilimleri Enstitusu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2024

29. Naringin protects against colistin-induced sciatic nerve damage by reducing oxidative stress, apoptosis and inflammation damage.

Author

YILMAZ, Selçuk, KÜÇÜKLER, Sefa, ŞİMŞEK, Hasan, AYGÖRMEZ, Serpil, and KANDEMİR, Fatih Mehmet

Subjects
*SCIATIC nerve, *OXIDATIVE stress, *NARINGIN, *SCIATIC nerve injuries, *POISONS
Abstract

Colistin is used in treatment against gram-negative bacteria. It causes toxic effects due to oxidative stress in a dose-dependent manner. Naringin is a flavonoid with strong antioxidant properties found naturally in many plants, especially citrus fruits. This study aimed to determine the protective effects of NRG in CLS-induced sciatic nerve injury. Thirty-five male Spraque Sprague rats were randomly divided into five groups: control, NRG, CLS, CLS+NRG 50, and CLS+NRG 100. CLS was administered intraperitoneally at a 15 mg/kg dose for seven days. NRG was administered orally at 50 or 100 mg/kg doses for seven days. Sciatic nerve tissues were collected and analyzed for oxidative stress markers, inflammation, and apoptosis damage levels by biochemical methods. CLS caused toxic damage in sciatic nerve tissue by increasing lipid peroxidation (MDA) and decreasing antioxidant levels (SOD, CAT, GPx, and GSH); increasing NF-B, TNF-α, nNOS release; increasing apoptotic factor (Caspase-3); decreasing HO-1 and nCAM; and inducing 8-OHdG, MAPK and GFAP (p<0.05). NRG, on the other hand, reversed all these changes in sciatic nerve tissue, and reduced CLS-induced oxidative stress damage, inflammatory damage and apoptotic damage (p<0.05). These effects were more effective at the 100 mg/kg dose of NRG than at the 50 mg/kg dose (p<0.05). NRG showed a protective effect against CLS-induced sciatic nerve toxicity. [ABSTRACT FROM AUTHOR]

Published
2024
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30. Determination of the Effects of Helichrysum Plicatum DC. Subspecies Plicatum Ethanol Extract on Thallium Sulfate Induced Testicular Toxicity in Rat.

Author

Ömür, Ali Doğan, Yıldırım, Betül Apaydın, Küçükler, Sefa, Mokhtare, Behzad, Karataş, Özhan, Özkaraca, Mustafa, and Akarsu, Serkan Ali

Subjects
PHYTOTHERAPY, THALLIUM, BIOLOGICAL models, SEMEN analysis, BIOPSY, IN situ hybridization, ETHANOL, SULFATES, OXIDATIVE stress, DESCRIPTIVE statistics, PLANT extracts, RATS, EXPERIMENTAL design, IMMUNOHISTOCHEMISTRY, GENE expression, LIPID peroxidation (Biology), TESTICULAR diseases, TESTIS, ANTIOXIDANTS, ANIMAL experimentation, SPERM motility, COMPARATIVE studies, DATA analysis software, TOXICITY testing
Abstract

Copyright of Van Health Sciences Journal / Van Sağlık Bilimleri Dergisi is the property of Van Yuzuncu Yil University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2024
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32. Effects of Vitis vinifera L. cv. "Merlot" Seed Extract Against Thallium (I) Sulfate-Induced Reproductive Damage in Male Rats.

Author

ÖMÜR, Ali Doğan, APAYDIN YILDIRIM, Betül, MOKHTARE, Behzad, KÜÇÜKLER, Sefa, MENDİL, Ali Sefa, GEZER, Arzu, and AKARSU, Serkan Ali

Subjects
VITIS vinifera, GRAPE seed extract, THALLIUM, ANIMAL reproduction, OXIDATIVE stress
Abstract

Copyright of Veterinary Sciences & Practices is the property of Ataturk University Coordinatorship of Scientific Journals and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2023
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33. Sıçan Dalak Dokusunda Akrilamidin İndüklediği Oksidatif Stres, İnflamasyona ve Apoptoza Karşı Morinin Koruyucu Etkileri: Biyokimyasal ve Histopatolojik Bir Yaklaşım.

Author

AKARAS, Nurhan, KANDEMİR, Fatih Mehmet, ŞİMŞEK, Hasan, KÜÇÜKLER, Sefa, and OĞUZ KABAYEL, Rabia

Subjects
OXIDATIVE stress, ACRYLAMIDE, SPLEEN, RATS, INFLAMMATION
Abstract

Copyright of Firat Universitesi Saglik Bilimleri Veteriner Dergisi is the property of Firat Universitesiu, Saglik Bilimleri Enstitusu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2023

36. Protective effects of zingerone against sodium arsenite-induced lung toxicity: A multi-biomarker approach.

Author

Şimşek, Hasan, Küçükler, Sefa, Gür, Cihan, İleritürk, Mustafa, Aygörmez, Serpil, and Kandemir, Fatih Mehmet

Subjects
*LUNGS, *SODIUM arsenite, *OXIDATIVE stress, *SODIUM, *HONEY plants
Abstract

Objective(s): Sodium arsenite (SA) exposure is toxic to the body. Zingerone (ZNG) is a flavonoid with many biological properties found naturally in honey and plants. This study aimed to determine the effects of ZNG on SA-induced rat lung toxicity. Materials and Methods: Thirty-five male Sprague rats were divided into Control, SA, ZNG, SA+ZNG25, and SA+ZNG50 groups (n=7). SA 10 mg/kg and ZNG were administered at two doses (25 and 50 mg/kg) (orally, 14 days). Analysis of oxidative stress, inflammation damage, apoptosis damage, and autophagic damage markers in lung tissue were determined by biochemical and histological methods. Results: The administration of ZNG reduced oxidative stress by increasing SA-induced decreased antioxidant enzyme activities, increasing Nrf-2, HO-1, and NQO1, and decreasing MDA level. ZNG administration reduced inflammation marker levels. Anti-apoptotic Bcl-2 increased and apoptotic Bax and Caspase-3 decreased with ZNG. ZNG promoted the regression of autophagy by reducing Beclin-1, LC3A, and LC3B levels. Conclusion: Evaluating all data showed that SA caused toxic damage to lung tissue by increasing inflammation, apoptosis, autophagy, and oxidant levels, whereas ZNG had a protective effect by reducing this damage. [ABSTRACT FROM AUTHOR]

Published
2023
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38. The investigation of the effect of fraxin on hepatotoxicity induced by cisplatin in rats

Author

Ekinci̇-Akdemi̇r, Fazile Nur, Bi̇ngöl, Çiğdem, Yıldırım, Serkan, Kandemi̇r, Fatih Mehmet, Küçükler, Sefa, and Sağlam, Yavuz Selim

Subjects
Oxidative stress, Hepatotoxicity, Original Article, Apoptosis, Cisplatin, Fraxin
Abstract

Objective(s): This study was designed to assess the effect of fraxin which has various biological properties against liver injury induced by cisplatin. Materials and Methods: In our study, 24 Wistar albino rats were randomly assigned to control, fraxin, cisplatin, and fraxin+cisplatin groups. Cisplatin 12 mg/kg IP and fraxin 40 mg/kg orally were applied. When the experiment ended, the rats were sacrificed and the liver tissues were taken rapidly. Liver tissue specimens were maintained under appropriate conditions. Later, biochemical, histopathological, and immunohistochemical evaluations were performed. Results: According to our biochemical findings, oxidant parameters increased while antioxidant parameters decreased in cisplatin group compared with control group. Antioxidant parameters increased but oxidant parameters decreased in fraxin + cisplatin group compared with the cisplatin group. Immunohistochemical evaluations showed that the expressions of TNF-α and Caspase-3 were negative in control and fraxin groups, whereas severe levels were found in the cisplatin group. However, it was determined that the expressions of TNF-α and Caspase-3 were in mild levels in fraxin + cisplatin treatment group. In addition, it was observed that the increase of pathological markers such as coagulation necrosis, hydropic degeneration, dilatation in sinusoid, and hyperemia in the cisplatin group were compatible with our biochemical and immunohistochemical findings. Conclusion: Biochemical, immunohistochemical, and histopathological results revealed that fraxin was effective in relieving cisplatin-induced liver damage.

Published
2020

39. Oksaliplatin Kaynaklı Testis Hasarı Üzerine Likopenin Etkilerinin Araştırılması

Author

KÜÇÜKLER, Sefa and KANDEMİR, Fatih Mehmet

Subjects
Likopen,oksaliplatin,oksidatif Stres,rat, Farmakoloji ve Eczacılık, Veteriner Hekimlik, Veterinary Sciences, Pharmacology and Pharmacy, Lycopene,oxaliplatin,oxidative Stress,rat
Abstract

Oxaliplatin (Olp) is a drug widely used in the treatment of advanced colorectal cancers. Compared to other platinum derivatives, oxaliplatin causes only mild haematological and gastrointestinal toxicity. Lycopene (Lcp), an acyclic hydrocarbon carotenoid found in tomatoes and their products, is a potent antioxidant and has been shown to have anticancer properties in animal models. This study aims to evaluate the protective effects of Lcp against Olp-induced testicular toxicity in rats. Male Sprague Dawley rats were used in the study and 5 experimental groups were formed: 1-control group, 2-Lycopene (Lcp) administered group, 3-Oxaliplatin (Olp) administered group, 4-Oxaliplatin + lycopene 2 mg/kg (Olp+Lcp2) administered group. group and 5-oxaliplatin + lycopene 4 mg/kg (Olp+Lcp4) administered group. On days 1 and 2, and days 5 and 6, 30 minutes after lycopene administration, oxaliplatin is dissolved in 5% dextrose ata dose of 4 mg/kg and administered i.p. was applied as Tissue malondialdehyde (MDA), glutathione (GSH) levels, glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (Cat) activities were determined biochemically. While MDA levels increasedin testicular tissue in the oxaliplatin group, GSH, GPx, SOD and CAT values decreased. Different doses of lycopene administered with oxaliplatin decreased MDA levels and increased GSH, GPx, SOD and CAT activities. In this study, it was determined that lycopene has a protective feature against testicular damage induced by oxaliplatin., Oksaliplatin (Olp) ilerlemiş kolorektalkanserlerin tedavisinde yaygın olarak kullanılan bir ilaçtır. Diğer platin türevlerine göre oksaliplatin, sadece hafif bir hematolojik ve gastrointestinal toksisiteye neden olmaktadır. Domateslerde ve ürünlerindebulunan asiklik bir hidrokarbon karotenoidolan likopen (Lcp), güçlü bir antioksidandır ve hayvan modellerinde antikanser özellikleri gösterilmiştir. Bu çalışma sıçanlarda Lcp’nin Olp ile indüklenen testis toksisitesine karşı koruyucu etkilerini değerlendirmeyi amaçlamaktadır. Araştırmada erkek Sprague Dawley sıçanları kullanıldı ve 5 deney grubu oluşturuldu: 1-kontrol grubu, 2-Likopen (Lcp) uygulanan grup, 3-Oksaliplatin (Olp) uygulanan grup, 4-Oksaliplatin + likopen 2 mg/kg (Olp+Lcp2) uygulanan grup ve 5-oksaliplatin + likopen 4 mg/kg (Olp+Lcp4) uygulanan grup. 1 ve 2. günler ile 5 ve 6. günler likopen uygulamasından 30 dakika sonra oksaliplatin 4 mg/kg dozunda %5 dektrozda çözülerek i.p. olarak uygulandı. Doku malondialdehit (MDA), glutatyon (GSH) düzeyleri, glutatyon peroksidaz (GPx), süperoksit dismutaz (SOD) ve katalaz (KAT) aktiviteleri biyokimyasal olarak belirlendi. Testis dokusunda oksaliplatin grubunda MDA düzeyleri yükselirken, GSH, GPx, SOD ve Kat değerleri azaldı. Likopenin oksaliplatin ile uygulanan farklı dozları ise MDA düzeyini azaltırken, GSH, GPx, SOD ve KAT aktivitelerini artırdı. Bu çalışma ile oksaliplatin ile oluşturulan testis hasarına karşı likopenin koruyucu özelliğinin olduğu tespit edilmiştir.

Published
2022

46. Ratlarda i̇zoniazid kaynaklı akciğer hasarına karşı krisinin etkileri

Author

Küçükler, Sefa, Özdemi̇r, Selçuk, Çomaklı, Selim, and Kandemi̇r, Fatih Mehmet

Subjects
Oksidatif Stres, Krisin, Akciğer, İzoniazid
Abstract

Bu çalışmanın amacı; tüberküloz tedavisinde yaygın olarak kullanılan izoniazid (İZN) kaynaklı akciğer hasarına karşı doğal flavonoidlerden olan krisin (KRS)’in etkilerinin araştırılmasıdır. Çalışmada Spraque Dawley cinsi 35 adet erkek rat rastgele 5 gruba ayrıldı: Kontrol grubu, İZN uygulanan grup, KRS 50 mg/kg uygulanan grup, İZN+ KRS 25 mg/kg uygulanan grup ve İZN+ KRS 50 mg/kg uygulanan grup. İZN’nin glutatyon peroksidaz (GPx), süperoksit dismutaz (SOD) ve katalaz (KAT) gibi antioksidan enzim aktivitelerini ve glutatyon (GSH) düzeylerini azaltıp, lipid peroksidasyonunu (LPO) artırarak oksidatif hasara neden olduğu belirlendi. Ayrıca İZN ile kombine uygulanan KRS uygulamasının GSH seviyesini ve antioksidan enzim aktivitelerini artırdığı, lipid peroksidasyonunu ise azalttığı ettiği tespit edildi. Çalışmada incelenen nükleer faktör eritroid 2 ile ilişkili faktör 2 (Nrf-2) ve hem oksijenaz-1 (HO-1) seviyelerinin İZN grubunda gen ekspresyonu düzeyinde, nükleer faktör kappa B (NF-κB) ekspresyonunu ise immunhistokimyasal incelemede arttığı tespit edilmiş, buna karşın KRS uygulamasının bu belirteçlerin düzeylerinde azalmaya neden olduğu gözlenmiştir. Birlikte ele alındığında, bu sonuçlar KRS'in oksidan-antioksidan dengesini koruyarak ve NF-κB, Nrf-2 ve HO-1 ekspresyonlarını azaltarak İZN’nin neden olduğu akciğer toksisitesinde faydalı etkilere sahip olduğunu düşündürmektedir. The aim of the study was to investigate the effects of chrysin (CH), one of the natural flavonoids, against isoniazid lung damage caused by isoniazid (INH), which was widely used in the treatment of tuberculosis. Male Sprague-Dawley rats were randomly divided into five groups: a control group, INH-treated group, CH alone treated group 50 mg / kg, INH + CH 25 mg / kg treated group, and INH+ CH 50 mg / kg treated group. It was determined that INH caused oxidative damage by decreasing antioxidant enzyme activities such as glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) and increasing lipid peroxidation (LPO). In addition, it was found that the administration of CH to INH-treated rats increased GSH level and antioxidant enzyme activities, and decreased lipid peroxidation. It was observed that the nuclear factor erythroid 2 related factor 2 (Nrf-2) and oxygenase-1 (HO-1) expression levels were up-regulated in the INH-treated group, and the expression of NF-κB increased in the INH-treated group in the immunohistochemical examination, and the CH administration, on the other hand, decreased the levels of these markers. Taken together, these results suggested that CH had beneficial effects in INH-induced lung toxicity by maintaining the oxidant-antioxidant balance and decreasing NF-κB, Nrf-2, and HO-1 expressions.

Published
2020

47. Effects of Carvacrol Against Cadmium-Induced Stomach Toxicity in Rats

Author

KÜÇÜKLER, Sefa, ÖZDEMİR, Selçuk, KANDEMİR, Fatih, and ÇAĞLAYAN, Cüneyt

Subjects
Veterinary, Cadmium,Carvacrol,Stomach,Oxidative stress, Veteriner Hekimlik, Kadmiyum,Karvakrol,Mide,Oksidatif stres
Abstract

Sunulan çalışmanın amacı; ağır metallerden olan kadmiyumun (Cd) neden olduğu mide toksisitesine karşı karvakrol (Krv)’nin etkilerinin araştırılmasıdır. Çalışmada Spraque Dawley cinsi 35 adet erkek rat rastgele 5 gruba ayrıldı: Kontrol grubu, Cd uygulanan grup, Krv 50 mg kg-1 uygulanan grup, Cd + Krv 25 mg kg-1 uygulanan grup ve Cd + Krv 50 mg kg-1 uygulanan grup. Cd’nin glutatyon peroksidaz (GPx), süperoksit dismutaz (SOD) ve katalaz (KAT) gibi antioksidan enzim aktivitelerini ve glutatyon (GSH) düzeylerini azaltıp, lipid peroksidasyonunu (LPO) artırarak oksidatif hasara neden olduğu belirlendi. Ayrıca Cd ile kombine uygulanan Krv uygulamasının GSH seviyesini ve antioksidan enzim aktivitelerini arttırdığı, lipid peroksidasyonunu ise azalttığı tespit edildi. Çalışmada incelenen glikoz düzenleyici protein 78 (GRP78) mRNA transkipt seviyesinin Cd grubunda önemli şekilde arttığı, Krv uygulamasının ise bu gene ait ekspresyon seviyesini azalttığı belirlendi. Mide dokusunda Cd toksikasyonu aktive edici transkripsiyon faktör 6 (ATF6) ekspresyonunu arttırdığı, Krv uygulaması ile bu gene ait ekspresyonda düşüş meydana geldiği saptandı.Sonuç olarak; Cd kaynaklı mide toksisitesinde Krv’nin yararlı etkilerinin olduğu oksidan-antioksidan denge ile GRP78 ve ATF6 ekspresyonları incelenerek tespit edildi., The aim of this study is investigation of the effects of carvacrol (Crv) against stomach toxicity caused by cadmium (Cd), which is a heavy metal. In the study, 35 male rats of Spraque Dawley were randomly divided into 5 groups: the control group, the group that received Cd, the group recevied Crv 50 mg kg-1, the group that received Cd + Crv 25 mg kg-1, and the group that received Cd + Crv 50 mg kg-1. It has been determined that Cd causes oxidative damage by decreasing antioxidant enzyme activities such as glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT), and increasing lipid peroxidation (LPO). In addition, it was found that Crv administration combined with Cd increased GSH level and antioxidant enzyme activities and decreased lipid peroxidation. It was determined that the level of glucose regulated protein 78 (GRP78) mRNA transcript examined in the study increased significantly in the Cd group, while Crv application decreased the expression level of this gene. It was determined that Cd toxicity in the stomach tissue increased activating transcription factor 6 (ATF6) expression and that the expression of this gene decreased with the recevied of Crv.As a result, it has been determined by examining the oxidant-antioxidant balance with GRP78 and ATF6 expressions that Crv has beneficial effects on Cd-induced stomach toxicity.

Published
2020

48. Alterations in Enzyme Activity of Carbonic Anhydrase, 6-phosphogluconate Dehydrogenase and Thioredoxin Reductase in Rats Exposed to Doxorubicin and Morin

Author

AĞGÜL, Ahmet Gökhan, KUZU, Müslüm, KANDEMİR, Fatih Mehmet, KÜÇÜKLER, Sefa, ÇAĞLAYAN, Cüneyt, and Belirlenecek

Subjects
Therapeutic Applications, Protection, Toxicity, Inhibitors, Doxorubicin,Morin,Carbonic Anhydrase,6-phosphogluconate Dehydrogenase,Thioredoxin Reductase, Induced Apoptosis, Activation, Expression, Induced Cardiotoxicity, Carbonic Anhydrase, Metabolism, Morin, Doxorubicin, 6-phosphogluconate Dehydrogenase, Thioredoxin Reductase, Profiles
Abstract

Objectives: Carbonic anhydrase (CA), 6-phosphogluconate dehydrogenase (6PGD) and thioredoxin reductase (TrxR) enzymes are the essential biological molecules needed for metabolic processes in all living cells. This study was designed to investigate the activities of CA, 6PGD and TrxR enzymes in the brain, kidney, liver, heart and testis tissues of the rats exposed to doxorubicin (DOX) and morin. Methods: Male Wistar albino rats were randomly divided into three groups as control, morin and DOX, each of them containing 7 rats. At the end of the experimental procedure, CA, 6PGD, and TrxR enzyme activities in tissues of rats were determined spectrophotometrically. Results: In our study, we observed that DOX activated CA enzyme in liver and kidney tissues while inhibiting CA enzyme in the other tissues, activated 6PGD enzyme in the kidney, liver and heart tissues, and inhibited the TrxR enzyme in all the tissues. In addition, morin activated CA enzyme in the liver tissue while inhibiting CA enzyme in the brain, heart and testis tissues. Morin activated 6PGD enzyme activity while it inhibited TrxR enzyme in all the tissues. Conclusion: The findings showed that doxorubicin and morin had similar properties in the tissues as to their effect on enzyme activities., Agri Ibrahim Cecen University Scientific Research Projects Unit [ECZF.17.001], A part of this research was supported by Agri Ibrahim Cecen University Scientific Research Projects Unit [Grant no ECZF.17.001].

Published
2020

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