ALLOKSAN CHAQIRGAN QANDLI DIABETDA OKSIDLOVCHI STRESS VA ANTIOKSIDANT HIMOYA TIZIMI O'RTASIDAGI BOG'LIQLIK: BIOKIMYOVIY VA PATOGENETIK JIHATLAR
DOI:
https://doi.org/10.5281/zenodo.20823260Ключевые слова:
alloksan diabeti, oksidlovchi stress, antioksidant himoya, malon dialdegidi, superoksiddismutaza, katalaza, lipidlar peroksidlanishi, diabetik gepatopatiya, sitoliz, giperglikemiya.Аннотация
Ushbu tadqiqot alloksan yordamida modellashtrilgan eksperimental qandli diabet sharoitida jigar to'qimasidagi lipidlar peroksidlanishi (LPO) intensivligi, antioksidant fermentlar — superoksiddismutaza (SOD) va katalaza — faolligini hamda sitoliz markerlarini (ALT, AST) kompleks biokimyoviy tahlil asosida o'rganishga qaratilgan. Tajribalar vazni 180–220 g bo'lgan sog'lom oq kalamushlarda o'tkazildi. Hayvonlar nazorat (n=12) va alloksan-diabetik (n=12) guruhlarga ajratildi. Alloksan monohidrat 150 mg/kg dozasida qorin bo'shlig'iga yuborildi. 72 soatdan so'ng glikemiya ≥11 mmol/l bo'lgan hayvonlar tajribaga kiritildi. MDA miqdori TBK-usulida, SOD faolligi nitrosiniy tetrazoliy ingibitsiyasi, katalaza — ammoniy molibdat kompleksi, ALT/AST — Reytman–Frenkel usulida aniqlandi. Diabet guruhida MDA darajasi 3,93 baravar oshdi (1,24±0,09 dan 4,87±0,21 nmol/mg oqsilgacha, p<0,001). SOD faolligi 50,0% pasaydi (18,6±0,8 dan 9,3±0,6 U/mg oqsilgacha, p<0,001), katalaza faolligi 53,2% kamaydi (42,3±2,1 dan 19,8±1,4 mmol H₂O₂/min/mg oqsilgacha, p<0,001). ALT va AST faolligi mos ravishda 2,98 va 3,13 barobarga oshib, kuchli sitoliz sindromini ko'rsatdi.Библиографические ссылки
International Diabetes Federation. IDF Diabetes Atlas, 10th Edition. — Brussels: IDF, 2021. — 184 p. URL: https://diabetesatlas.org
Powers A.C. Diabetes mellitus: diagnosis, classification, and pathophysiology // Harrison's Principles of Internal Medicine. — 20th ed. — New York: McGraw-Hill, 2018. — P. 2850–2903.
Bhattamisra S.K., Khang G.A., Bhargava P. et al. Diabetes mellitus and oxidative stress: a comprehensive review // Biomedicine and Pharmacotherapy. — 2021. — Vol. 143. — P. 112087. DOI: 10.1016/j.biopha.2021.112087
Lenzen S. The mechanisms of alloxan- and streptozotocin-induced diabetes // Diabetologia. — 2008. — Vol. 51, No. 2. — P. 216–226. DOI: 10.1007/s00125-007-0886-7
Gerber P.A., Rutter G.A. The role of oxidative stress and hypoxia in pancreatic beta-cell dysfunction in diabetes mellitus // Antioxidants & Redox Signaling. — 2017. — Vol. 26, No. 10. — P. 501–518. DOI: 10.1089/ars.2016.6755
Ojo O.A., Aminu A., Ayinde O. et al. Oxidative stress markers in alloxan-induced diabetic rats: role of liver enzyme activities and antioxidant status // Biomedicine & Pharmacotherapy. — 2022. — Vol. 149. — P. 112878.
Azizov Sh.M., Karimov A.A. Alloksan diabetida jigar to'qimasida oksidlovchi stress ko'rsatkichlari va antioksidant fermentlar dinamikasi // Patologiya jurnali. — 2023. — №3. — B. 41–46.
Brownlee M. Biochemistry and molecular cell biology of diabetic complications // Nature. — 2001. — Vol. 414, No. 6865. — P. 813–820. DOI: 10.1038/414813a
Nishikawa T., Edelstein D., Brownlee M. The missing link: a single unifying mechanism for diabetic complications // Kidney International Supplement. — 2000. — Vol. 77. — P. S26–S30.
Davi G., Falco A., Patrono C. Lipid peroxidation in diabetes mellitus and antioxidant defenses // Antioxidants & Redox Signaling. — 2005. — Vol. 7, No. 1–2. — P. 256–268.
Toshov Sh.S., Aliev X.A. Eksperimental qandli diabetda erkin radikalli jarayonlar va jigar sitoliz fermentlari o'rtasidagi bog'liqlik // O'zbekiston tibbiyot jurnali. — 2022. — №2. — B. 48–53.
Sies H., Berndt C., Jones D.P. Oxidative stress // Annual Review of Biochemistry. — 2017. — Vol. 86. — P. 715–748. DOI: 10.1146/annurev-biochem-061516-045037
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