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Journals / Muğla Sıtkı Koçman Üniversitesi Tıp Dergisi / 2026 / Volume: 13 Issue: 2

Biochemical Antioxidant Effects of Ellagic Acid Against Di-(n)-butyl Phthalate–Induced Oxidative Stress in Rat Brain Tissue

Sıçan Beyin Dokusunda Di-(n)-bütil Ftalat Kaynaklı Oksidatif Strese Karşı Elajik Asidin Biyokimyasal Antioksidan Etkileri

İdris Ayhan(PAMUKKALE ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0003-4625-7218
Neşe Başak Türkmen(İNÖNÜ ÜNİVERSİTESİ, ECZACILIK FAKÜLTESİ)0000-0001-5566-8321
Demet Döndü Kasım(PAMUKKALE ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0003-0343-1255
Osman Çiftçi(PAMUKKALE ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0001-5755-3560
Pages
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Publication Date
2026-08-27
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These findings indicate that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.

📌 3 Key Takeaways

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Objective & Hypothesis:Di-n-butyl phthalate (DBP), a widely used plasticizer, induces oxidative stress and neurotoxicity through the generation of reactive oxygen species.
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Key Findings & Data:DBP was administered orally at a dose of 500 mg/kg/day, while EA was given by gavage at 2 mg/kg/day for four weeks.
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Conclusion & Impact:These findings indicate that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Antioxidant Enzymes · Di-n-butyl Phthalate · Ellagic Acid

Abstract

Di-n-butyl phthalate (DBP), a widely used plasticizer, induces oxidative stress and neurotoxicity through the generation of reactive oxygen species. Ellagic acid (EA), a natural polyphenolic antioxidant, may counteract these effects. This study aimed to evaluate the protective role of EA against DBP-induced oxidative brain injury. Thirty-two male rats were randomly divided into four groups: Control, DBP, EA, and DBP+EA. DBP was administered orally at a dose of 500 mg/kg/day, while EA was given by gavage at 2 mg/kg/day for four weeks. Oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities were analyzed in brain tissue. DBP exposure significantly increased TBARS levels while decreasing GSH and SOD activities, indicating lipid peroxidation and antioxidant depletion. In contrast, CAT activity was elevated, suggesting a compensatory enzymatic response to excess hydrogen peroxide. EA treatment markedly attenuated oxidative damage by restoring GSH and SOD levels and normalizing CAT activity. These findings indicate that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.

Özet

Di-n-butil ftalat (DBP), yaygın olarak kullanılan bir plastikleştirici olup, reaktif oksijen türlerinin (ROS) oluşumu yoluyla oksidatif stres ve nörotoksisiteye neden olur. Doğal bir polifenolik antioksidan olan elajik asit (EA), bu etkileri dengeleyebilir. Bu çalışmada, EA’nın DBP kaynaklı oksidatif beyin hasarına karşı koruyucu rolü araştırılmıştır. Otuz iki erkek sıçan rastgele dört gruba ayrılmıştır: Kontrol, DBP, EA ve DBP+EA. DBP, oral yolla 500 mg/kg/gün dozunda, EA ise dört hafta boyunca gavaj yoluyla 2 mg/kg/gün dozunda uygulanmıştır. Beyin dokusunda tiyobarbitürik asit reaktif maddeleri (TBARS), indirgenmiş glutatyon (GSH), süperoksit dismutaz (SOD) ve katalaz (CAT) aktivitelerini kapsayan oksidatif stres parametreleri analiz edilmiştir. DBP uygulaması, lipid peroksidasyonunu ve antioksidan tükenmesini yansıtarak TBARS düzeylerini anlamlı şekilde artırmış, GSH ve SOD aktivitelerini azaltmıştır. Buna karşın, CAT aktivitesi artmış olup aşırı hidrojen peroksite karşı gelişen kompanse edici bir enzimatik yanıtı düşündürmektedir. EA tedavisi, GSH ve SOD düzeylerini geri kazandırarak ve CAT aktivitesini normale döndürerek oksidatif hasarı belirgin şekilde hafifletmiştir. Bu bulgular, DBP’nin lipid peroksidasyonu yoluyla redoks homeostazını bozduğunu, EA’nın ise antioksidan savunmayı yeniden düzenleyerek oksidatif nörotoksisiteye karşı koruma sağladığını göstermektedir.

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Cite This Article

Ayhan, İ., Türkmen, N. B., Kasım, D. D., Çiftçi, O. (2026). Biochemical Antioxidant Effects of Ellagic Acid Against Di-(n)-butyl Phthalate–Induced Oxidative Stress in Rat Brain Tissue. Muğla Sıtkı Koçman Üniversitesi Tıp Dergisi, Volume: 13 Issue: 2. https://doi.org/10.47572/muskutd.1804319

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