KaydedilenlerDerginizi ekleyin

Dergiler / Journal of Cellular Neuroscience and Oxidative Stress / 2016 / Cilt: 8 - Sayı: 2

Melatonin reduces lens oxidative stress level in STZ-induced diabetic rats through supporting glutathione peroxidase and reduced glutathione values

Mehmet Cemal KAHYA
Mustafa NAZIROĞLU
Sayfa
588–594
Yayın Tarihi
2016-12-31
DOI
—
🏛️Bu makalenin bibliyografik verileri ve tam metin bağlantısı DergiPark üzerinden sağlanmıştır.
DergiPark Kaydı ↗
✨

Yapay Zeka Hızlı Bakış & Çıkarımlar

AI Insight
⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

In conclusion, the present study shows that melatonin induced protective effects against diabetes-induced lens oxidative injury through up-regulation of the GSH and GPx values but down-regulation of oxidative stress.

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:Hyperglycemia plays a critical role in the development and progression of diabetic cataract oxidative injuries via the increased reactive oxygen species (ROS) production.
📊
Temel Bulgular & Veri:The third and fourth groups received intraperitoneal 10 mg/kg melatonin for 2 weeks.
💡
Sonuç & Katkı:In conclusion, the present study shows that melatonin induced protective effects against diabetes-induced lens oxidative injury through up-regulation of the GSH and GPx values but down-regulation of oxidative stress.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Diabetes · Glutathione · Lens

Abstract

Hyperglycemia plays a critical role in the development and progression of diabetic cataract oxidative injuries via the increased reactive oxygen species (ROS) production. Melatonin has been considered a potent strong antioxidant that detoxifies a variety of ROS in many metabolic diseases. The present study was conducted to explore whether melatonin administration protects against diabetic lens oxidative injuries through modulation of reduced glutathione (GSH) and glutathione peroxidase (GPx) systems in streptozotocin (STZ)-induced diabetic rats. Thirty two rats were equally divided into four groups as control, STZ, melatonin and STZ and melatonin. The third and fourth groups received intraperitoneal 10 mg/kg melatonin for 2 weeks. For induction of diabetes in the second and fourth groups, intraperitoneal STZ (45 mg/kg) was given. Lipid peroxidation (MDA), total oxidant status and intracellular ROS levels in the lens were increased in STZ group although they were decreased by melatonin treatment. GPx activity, GSH concentration and total antioxidant status (TAS) were lower in STZ group than in control. However, the GSH concentration, GPx activity and TAS levels were recovered by melatonin. TAS was also higher in melatonin group than in the STZ and melatonin groups. In conclusion, the present study shows that melatonin induced protective effects against diabetes-induced lens oxidative injury through up-regulation of the GSH and GPx values but down-regulation of oxidative stress.

🔖

Bu Makaleye Atıf Yap

KAHYA, M. C., NAZIROĞLU, M. (2016). Melatonin reduces lens oxidative stress level in STZ-induced diabetic rats through supporting glutathione peroxidase and reduced glutathione values. Journal of Cellular Neuroscience and Oxidative Stress, Cilt: 8 - Sayı: 2, 588–594. https://ajindex.com/articles/827323

📄 Tam Metin PDF Okuyucu

📄

PDF görüntüleyici hazırlanıyor...

Kaynakça (10)

  1. Akash MS, Rehman K, Tariq M, Chen S. 2015. Zingiber officinale and Type 2 diabetes mellitus: evidence from experimental studies. Crit Rev Eukaryot Gene Expr. 25, 91-112.
  2. Balestri F, Cappiello M, Moschini R, Rotondo R, Abate M, Del-Corso A, Mura U. 2015. Modulation of aldose reductase activity by aldose hemiacetals. Biochim Biophys Acta. 1850, 2329-2339.
  3. Dilek M, Naziroğlu M, Baha Oral H, Suat Ovey I, Küçükayaz M, Mungan MT, Kara HY, Sütçü R. 2010. Melatonin modulates hippocampus NMDA receptors, blood and brain oxidative stress levels in ovariectomized rats. J Membr Biol. 233, 135-142.
  4. DU SC, Ge QM, Lin N, Dong Y, Su Q. 2012. ROS-mediated lipopolysaccharide-induced apoptosis in INS-1 cells by modulation of Bcl-2 and Bax. Cell Mol Biol (Noisy-le-grand). 58 Suppl, OL1654-1659. Ekmekcioglu C. 2006. Melatonin receptors in humans: biological role and clinical relevance. Biomed Pharm 60, 97-108. Erel O. 2004. A novel automated direct measurement method for total antioxidant capacity using a new generation, more stable ABTS radical cation. Clin Biochem 37, 277–285.
  5. Kador PF, Guo C, Kawada H, Randazzo J, Blessing K. 2014. Topical nutraceutical Optixcare EH ameliorates experimental ocular oxidative stress in rats. J Ocul Pharmacol Ther. 30(7), 593-602.
  6. Kahya MC, Nazıroğlu M, Çiğ B. 2017. Modulation of diabetes-induced oxidative stress, apoptosis, and Ca2+ entry through TRPM2 and TRPV1 channels in dorsal root ganglion and hippocampus of diabetic rats by melatonin and selenium. Mol Neurobiol. 54, 2345-2360.
  7. Khorsand M, Akmali M, Sharzad S, Beheshtitabar M. 2016. Melatonin reduces cataract formation and aldose reductase activity in lenses of streptozotocin-induced diabetic rat. Iran J Med Sci. 41, 305-313.
  8. Kovacic P, Somanathan R. 2008. Unifying Mechanism for Eye Toxicity: Electron transfer, reactive oxygen species, antioxidant benefits, cell signaling and cell Membranes. Cell Membr Free Radic Res 2, 56-69.
  9. Lawrence RA, Burk RF. 1976. Glutathione peroxidase activity in selenium-deficient rat liver. Biochem Biophys Res Commun 71, 952-958. Miranda-Díaz AG, Pazarín-Villaseñor L, Yanowsky-Escatell FG, Andrade-Sierra J. 2016. Oxidative stress in diabetic nephropathy with early chronic kidney disease. J Diabetes Res. 2016:7047238. Nazıroğlu M, Dikici DM, Dursun S. 2012. Role of oxidative stress and Ca(2+) signaling on molecular pathways of neuropathic pain in diabetes: Focus on TRP channels. Neurochem Res. 37, 2065-2075.
  10. Placer ZA, Cushman L, Johnson BC. 1966. Estimation of