MIMustafa Ileriturk

Mustafa Ileriturk

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Mustafa Ileriturk has a total of 50 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Open Access

    Effect of Borage Seed Oil Against Lead Acetate Neurotoxicity in Rats

    by Esra Aktas Senocak, Mustafa İlEritürk

    Lead (Pb) is a highly toxic heavy metal that has long been widely used in industry, agriculture, and the cosmetics sector. It also poses serious public health risks due to its tendency to accumulate in the body and to induce pronounced neurotoxicity, particularly by damaging the central nervous system via oxidative stress–mediated mechanisms. In the present study, the biochemical effects of lead acetate-induced neurotoxicity and the potential protective role of borage seed oil (Borago oil, BSO), known for its high medicinal and nutritional value, were evaluated in the brain tissue of rats by assessing oxidative stress parameters. A total of 30 Sprague Dawley rats were randomly divided into five groups. Neurotoxicity was induced by intraperitoneal administration of lead acetate at a dose of 20 mg/kg for 7 consecutive days. Borage oil was administered orally at doses of 50 and 100 mg/kg for 14 days. Malondialdehyde (MDA) levels in the rat brain tissue were measured using manual biochemical method, while the expression levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined by RT-PCR. Collectively, these findings indicate that borage seed oil partially alleviated Pb- associated oxidative stress alterationsin brain tissue, as evidenced by reduced lipid peroxidation (decreased MDA; p

  • Lipitler

    by Burcu Menekşe Balkan, Mustafa İlEritürk

    Lipitler, suda çözünmeyen ve polar olmayan çözücülerde çözünebilen heterojen bir biyomolekül grubudur. Bu gruba yağlar, mumlar, steroller, trigliseritler, fosfolipitler, glikolipitler ve yağda çözünen vitaminler gibi pek çok farklı bileşik dahil edilir. Yapısal olarak karbon, hidrojen ve oksijen elementlerinden oluşan lipitler, hücre zarlarının temel yapı taşlarını oluşturur, enerji deposu görevi görür ve çeşitli biyolojik süreçlerde sinyal iletimi, vitamin emilimi ve yalıtım gibi hayati roller üstlenir. Lipitlerin benzersiz kimyasal ve fiziksel özellikleri, onların biyolojik sistemlerde oldukça çeşitli işlevler üstlenmesini sağlar. Özellikle yağ asidi zincirlerinin uzunluğu, doygunluk derecesi ve omurga yapısı gibi faktörler, lipitlerin sınıflandırılmasında ve işlevsel özelliklerinde belirleyici olur. Ayrıca lipitlerin izomerik formları ve modifikasyonları da hücresel faaliyetleri doğrudan etkileyebilir. Lipitlerin enerji verimliliği oldukça yüksektir; gram başına karbonhidrat ve proteinlere göre yaklaşık iki kat daha fazla enerji sağlarlar, ancak bu enerjinin açığa çıkması daha yavaştır ve oksijene ihtiyaç duyar.Lipitler, yapısal çeşitliliklerine göre basit lipitler (örneğin trigliseritler ve mumlar), kompleks lipitler (fosfolipitler, glikolipitler, arkeal eter lipitler, steroller gibi) ve türev lipitler (eikosanoidler, terpenler) olarak sınıflandırılır. Trigliseritler vücutta başlıca enerji depolayıcı olarak görev yaparken, mumlar doğal koruyucu işlev görür. Hücre zarlarında yer alan kompleks lipitler, zarın akışkanlığını ve seçici geçirgenliğini düzenler. Fosfolipitler, gliserol veya sfingozin omurgası üzerinde fosfat ve çeşitli baş gruplar içeren moleküller olup, zar asimetrisinin ve sinyal iletiminin düzenlenmesinde önemli yer tutar. Ayrıca eikosanoidler gibi lipit türevleri lokal hormon olarak enflamasyon, ağrı ve immün yanıt gibi süreçleri düzenler. Esansiyel yağ asitleri olan omega-3 ve omega-6 yağları, organizma tarafından sentezlenemediğinden dışarıdan alınmalıdır; bu yağlar özellikle beyin fonksiyonu, kardiyovasküler sağlık ve bağışıklık sistemi için vazgeçilmezdir. Lipitlerin bu çok yönlü doğası, onları hem temel hücresel yapı taşları hem de dinamik biyokimyasal regülatörler haline getirir. Lipids are a heterogeneous group of biomolecules that are insoluble in water but soluble in nonpolar solvents. This group includes a wide variety of compounds such as fats, waxes, sterols, triglycerides, phospholipids, glycolipids, and fat-soluble vitamins. Structurally composed of carbon, hydrogen, and oxygen, lipids form the essential components of cell membranes, serve as energy reserves, and play critical roles in various biological processes such as signal transduction, vitamin absorption, and thermal insulation. Their unique chemical and physical properties enable lipids to perform highly diverse functions in biological systems. In particular, the length of fatty acid chains, degree of saturation, and backbone structure are key factors in lipid classification and functional properties. Additionally, the isomeric forms and modifications of lipids can directly influence cellular activity. Lipids are highly energy-efficient, providing nearly twice as much energy per gram as carbohydrates and proteins; however, the release of this energy is slower and requires oxygen.Based on their structural diversity, lipids are classified as simple lipids (e.g., triglycerides and waxes), complex lipids (e.g., phospholipids, glycolipids, archaeal ether lipids, and sterols), and derived lipids (e.g., eicosanoids and terpenes). Triglycerides primarily function as energy storage molecules in the body, while waxes serve as natural protective agents. Complex lipids in cell membranes regulate membrane fluidity and selective permeability. Phospholipids, which consist of a glycerol or sphingosine backbone attached to phosphate groups and various head groups, play a key role in maintaining membrane asymmetry and regulating signal transduction. Furthermore, lipid derivatives such as eicosanoids act as local hormones that regulate processes like inflammation, pain, and immune responses. Essential fatty acids, such as omega-3 and omega-6, must be obtained from the diet as they cannot be synthesized by the body; these lipids are crucial for brain function, cardiovascular health, and immune system integrity. The multifaceted nature of lipids makes them both fundamental structural elements of cells and dynamic biochemical regulators.

  • Biyokimya-I

    by Mahire Bayramoğlu Akkoyun, Meryem Şentürk, Barış Denk, Burcu Menekşe Balkan, Mustafa İlEritürk, Özkan Duru, Kıvanç İrAk, Emre Kaya, Filiz Kazak Akçakavak, Sedat Çetin, et al.

  • Open Access

    Carvacrol Coadministration Ameliorates Lambda‐Cyhalothrin‐Induced Peripheral Neuropathy in Rats: Behavioral and Molecular Evidence

    by Özge Kandemir, Mustafa İlEritürk, Cihan Gür, Nurhan Akaras, Hasan Şimşek, Selçuk Yılmaz, Fatih Mehmet Kandemir

    This study aimed to investigate the possible neuroprotective effects of Carvacrol (CRV) against Lambda‐cyhalothrin (CYH)‐induced peripheral neuropathy. Thirty‐five rats were divided into five groups: Control, CRV, CYH, CYH+CRV25, and CYH+CRV50. CRV 25 or 50 mg/kg and CYH 6.23 mg/kg were administered orally for 21 days. The effects of these treatments were evaluated by hot plate and rotarod tests, followed by molecular, biochemical, histopathological, and immunohistochemical analyses of sciatic nerve tissues. CYH administration significantly impaired both sensory and motor functions. CRV doses (25 mg/kg and 50 mg/kg) administered with CYH significantly improved these impairments ( p < 0.001). Additionally, CYH increased MDA levels and decreased antioxidants, while CRV treatment reversed these effects. CRV also suppressed inflammation ( p < 0.01), apoptosis ( p < 0.001), and endoplasmic reticulum stress ( p < 0.001), with the 50 mg/kg dose being more effective. Morphological and immunohistochemical analyses showed that CRV treatment partially repaired CYH‐induced nerve damage, with both doses reducing 8‐OHdG and beclin‐1 immunoreactions. The data revealed that CYH induced inflammation, oxidative stress, ER stress, and apoptosis in sciatic tissue, while CRV exhibited antioxidant, anti‐inflammatory, and antiapoptotic effects, reducing the damage and suggesting its potential as a supportive treatment for CYH‐induced sciatic damage.


  • Open Access

    Morin Attenuates Diclofenac‐Induced Hepatocellular Death Injury via Nrf2/Ho‐1/NQO1, Beclin‐1/LC3A/LC3B and p53/Bax/Caspase Signalling Pathways

    by Nurhan Akaras, Hasan Şimşek, Cihan Gür, Sefa Küçükler, Mustafa İlEritürk, Fatih Mehmet Kandemir

    Diclofenac (DF), a nonsteroidal and anti‐inflammatory drug, has limited use due to its adverse effects on the liver. On the other hand, morin, a bioflavonoid, has biological and pharmacological properties. This study aims to investigate whether morin may protect against diclofenac‐induced liver toxicity. For this purpose, morin (50 or 100 mg/kg) treatment was given orally to the rats for 5 days, and DF (50 mg/kg) was administered intraperitoneally on the 4th and 5th days of the study. Molecular, biochemical, immunohistochemical and histological methods were used to investigate cyclooxygenase enzymes, oxidative stress, apoptosis and autophagy in liver tissue. According to the data obtained, it was observed that DF caused oxidative stress, autophagy and apoptosis damage in liver tissues. Morin showed antioxidant properties, causing a decrease in MDA in hepatic tissue, an increase in the activities of endogenous antioxidants (glutathione peroxidase, superoxide dismutase and catalase) and GSH, HO‐1, Nrf2 and NQO1 mRNA levels. Moreover, morin reversed the changes in the levels of apoptotic and autophagic parameters such as bax, bcl‐2, cytochrome c, p53, Apaf‐1, caspase‐3, caspase‐6, caspase‐9, beclin‐1, LC3A, LC3B, MAPK14, MAP15, JNK. When the histopathological analysis results were examined, degenerative changes occurred in the livers of rats administered DF, while morin administration showed a morphological structure close to the control group. As a result, it was determined that oxidative stress, autophagy and apoptosis caused by DF were suppressed by morin, thus protecting the liver tissue from damage.


  • Open Access

    Hepatoprotective Effects of Royal Jelly Against Vincristine-Induced Hepatotoxicity in Rats: A Biochemical and Molecular Study

    by Rahime Erzincan, Cuneyt Caglayan, Fatih Mehmet Kandemir, Ebubekir İzol, Cihan Gür, Mustafa İleritürk

    Vincristine (VCR) is a chemotherapeutic agent classified as a vinca alkaloid. Royal jelly (RJ) is a significant bee product produced by worker bees, characterized by its high protein content. This study aims to investigate the protective effects of RJ against VCR-induced liver damage. VCR was intraperitoneally administered at a dose of 0.1 mg/kg body weight (b.w.) and RJ was orally administered at doses of 150 and 300 mg/kg b.w. Both treatments were applied to the rats on days 1–6 and 9–14. The composition of RJ was analyzed using LC-MS/MS, revealing the presence of 15 different phytochemical compounds with strong antioxidant properties. Serum samples obtained from the rats were analyzed for ALT, ALP, and AST levels. While these enzyme levels were significantly elevated in the VCR group, a notable reduction was observed following RJ administration. Additionally, SOD, CAT, GPx, and GSH antioxidant parameters, along with MDA levels, were evaluated in liver tissue samples. The results indicated a decrease in SOD, CAT, GPx, and GSH activities/levels and an increase in MDA levels in the VCR group. Furthermore, ELISA was used to assess JAK2, STAT3, and mTOR/PI3K/AKT signaling pathways. VCR administration led to a decrease in mTOR/PI3K/AKT levels and an increase in JAK2 and STAT3 levels. In addition, the mRNA transcription levels of inflammation (NF-κB, TNF-α, and IL-1β), endoplasmic reticulum (ER) stress (IRE-1, GRP78, PERK, and ATF-6), and autophagy markers (LC3A and LC3B) were examined. A significant increase in inflammation, ER stress, and autophagy-related markers was observed in the VCR-treated group. Lastly, the protein expression levels of Bax, Bcl-2, Caspase-3, and NF-κB were evaluated. VCR treatment increased Bax, Caspase 3, and NF-κB levels, whereas Bcl-2 levels were decreased. However, following RJ administration, all these parameters were reversed, demonstrating significant improvements. In conclusion, these findings suggest that RJ may exert a protective effect against VCR-induced liver damage.


  • Open Access

    Effect of familiar and unfamiliar riders on Cortisol, Oxytocin and Beta–endorphin levels in horses

    by Nergis Ulas, Omer Aydin, Sumeyye Baysal, Mustafa Ileriturk, Omer Eltas

    Stress response of the horse may be related to the behavioral and physiologic factors e.g., stress hormones. The aim of this study was to evaluate the different rider contact on the stress hormones of the horses that are used for javelin sport in a local riding club. Seven Arabian horses were ridden by familiar riders with the horses in the first and second weeks and by additional unfamiliar riders with the horses in the third and fourth weeks. Cortisol, oxytocin and beta–endorphin levels in sera samples and cortisol levels in saliva were measured before and after the riding. There was no statistical difference in serum cortisol and β–endorphin and salivary cortisol values between the groups with regard to the familiarity (P>0.05). Behavioral scoring did not differ between the groups. However, there was an increase in the oxytocin level of the horses ridden by the familiar riders in the second week compared with the first week (P<0.05). The horses did not respond stressfully associated with the hormone levels and behavioral changes; besides, they responded well to the familiar riders by elevating the oxytocin level. In conclusion, the horses used herein responded well to the familiar and unfamiliar riders with regard to potential stress factors. It has been therefore suggested that the familiarity towards the interaction between the human and the horse may not alter the physiological stress of the horses that are regularly ridden by various people in a riding club.


  • Open Access

    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

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

    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.


  • Open Access

    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

    by Serkan Ali Akarsu, Cihan Gür, Sefa Küçükler, Nurhan Akaras, Mustafa İlEritürk, Fatih Mehmet Kandemir

    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.


  • Top Cited Papers
    Open Access

    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

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

    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.