EFFECT OF LONG-TERM CENTRAL BLOCKING OF HORMONE RELEASE WITH TRIPTORELIN ON OXIDATIVE STRESS MARKER ACTIVITY IN THE LIVER OF RATS

Authors:

Abstract:

Over the past two decades, oxidative stress has been a significant concern among researchers in the field of biology worldwide. Stress can be defined as a process of altered biochemical homeostasis resulting from psychological, physiological, or environmental factors. Insufficient amounts of testosterone can worsen liver damage caused by obesity. Oxidative damage is linked to the cause of many diseases, such as cardiovascular disease, neuronal degeneration, and cancer, and also influences the aging process. The experiment was conducted on 60 sexually mature male white rats. The animals were divided into 3 groups. Group 1 – control rats injected with saline (10 animals). Group 2 – rats injected subcutaneously with diphereline (triptorelin) at a dose of 0.3 mg of active ingredient per kg of body weight with drug activity for 12 months (25 animals). Group 3 – rats that were administered a triptorelin solution at the rate of 0.3 mg of active ingredient per kg of body weight to simulate central deprivation of luteinizing hormone synthesis with the addition of quercetin to the diet using a gastric tube based on the body weight of the animals three times a week (25 animals). Triptorelin induces oxidative damage to hepatocytes by increasing the production of reactive oxygen species and decreasing the activity of antioxidant enzymes. Oxidative damage to liver cells begins at the molecular and cellular levels as early as the 1st month of observation. Additional administration of quercetin reduces manifestations of oxidative stress by increasing the activity of antioxidant enzymes and reducing the production of reactive oxygen species.

Keywords:

liver hepatocyte oxidative stress testosterone luteinizing hormone quercetin triptorelin

References:

1. Bahriy MM, Dibrova VA, Popadynets OH, Hryshchuk MI. Metodyky morfolohichnykh doslidzhen. Bahriy MM, Dibrova VA. redaktory. Vinnytsya: Nova knyha; 2016. 328. [in Ukrainian].
2. Bang WJ, Kim H, Oh CY, Jo JK, Cho JS, Shim M. Clinical significance of prostate volume and testosterone reduction on lower urinary tract symptoms in patients with prostate cancer undergoing androgen deprivation therapy. Sci Rep. 2022 Nov 2;12(1):18535. doi: 10.1038/s41598-022-21963-1.
3. Barjesteh F, Heidari-Kalvani N, Alipourfard I, Najafi M, Bahreini E. Testosterone, β-estradiol, and hepatocellular carcinoma: stimulation or inhibition? A comparative effect analysis on cell cycle, apoptosis, and Wnt signaling of HepG2 cells. Naunyn Schmiedebergs Arch Pharmacol. 2024 Aug;397(8):6121-6133. doi: 10.1007/s00210-024-03019-5.
4. Botté MC, Lerrant Y, Lozach A, Bérault A, Counis R, Kottler ML. LH down-regulates gonadotropin-releasing hormone (GnRH) receptor, but not GnRH, mRNA levels in the rat testis. J Endocrinol. 1999; 162(3): 409-415. doi:10.1677/joe.0.1620409.
5. Desai K, McManus JM, Sharifi N. Hormonal Therapy for Prostate Cancer. Endocr Rev. 2021 May 25;42(3):354-373. doi: 10.1210/endrev/bnab002.
6. Gur S, Alzweri L, Yilmaz-Oral D, Kaya-Sezginer E, Abdel-Mageed AB, Dick B, et al. Testosterone positively regulates functional responses and nitric oxide expression in the isolated human corpus cavernosum. Andrology. 2020 Nov; 8(6):1824-1833. doi: 10.1111/andr.12866.
7. Hao S, Östensson E, Eklund M, Grönberg H, Nordström T, Heintz E, et al. The economic burden of prostate cancer – a Swedish prevalence-based register study. BMC Health Serv Res. 2020 May 20;20(1):448. doi: 10.1186/s12913-020-05265-8.
8. Kimura T, Egawa S. Epidemiology of prostate cancer in Asian countries. Int J Urol. 2018 Jun; 25(6):524-531. doi: 10.1111/iju.13593.
9. Son SW, Lee JS, Kim HG, Kim DW, Ahn YC, Son CG. Testosterone depletion increases the susceptibility of brain tissue to oxidative damage in a restraint stress mouse model. J Neurochem. 2016 Jan;136(1):106-17. doi: 10.1111/jnc.13371.
10. Stetsuk YeV, Akimov OYe, Shepitko KV, Goltsev AN. Structural organization of stromal and parenchymal components of rat testes during central deprivation of testosterone synthesis on the 180 day of the experiment. World of medicine and biology. 2020; 72(2): 203-207. doi: 10.26724/2079-8334-2020-2-72-203-207.
11. Yassin A, AlRumaihi K, Alzubaidi R, Alkadhi S, Al Ansari A. Testosterone, testosterone therapy and prostate cancer. Aging Male. 2019 Dec; 22(4):219-227. doi: 10.1080/13685538.2018.1524456.
12. Yelinska AM, Akimov OYe, Kostenko VO. Role of AP-1 transcriptional factor in development of oxidative and nitrosative stress in periodontal tissues during systemic inflammatory response. Ukr. Biochem. J. 2019; 91(1): 80-85. doi:10.15407/ubj91.01.080.
13. Yang J, Lin S, Zhang Y, Wu G, Yang Q, Lv Q, et al. Taurine Improves Sexual Function in Streptozotocin-Induced Diabetic Rats. Adv Exp Med Biol. 2017; 975 Pt 1:307-318. doi: 10.1007/978-94-024-1079-2_27.
14. Wang D, Li Y, Zhai QQ, Zhu YF, Liu BY, Xu Y. Quercetin ameliorates testosterone secretion disorder by inhibiting endoplasmic reticulum stress through the miR-1306-5p/HSD17B7 axis in diabetic rats. Bosn J Basic Med Sci. 2022 Apr 1;22(2):191-204. doi: 10.17305/bjbms.2021.6299.
15. Zhang J, Gallaher J, Cunningham JJ, Choi JW, Ionescu F, Chatwal MS, et al. A Phase 1b Adaptive Androgen Deprivation Therapy Trial in Metastatic Castration Sensitive Prostate Cancer. Cancers (Basel). 2022 Oct 25;14(21):5225. doi: 10.3390/cancers14215225.

Publication:

«World of Medicine and Biology» Vol. 21 No. 91 (2025) , с. 177-180
УДК 611.36-018.1-06:615.357:577.432+615.322/.356-122.3

DOI:

https://doi.org/10.26724/2079-8334-2025-1-91-177-180