Journal of Exercise & Organ Cross Talk (Dec 2023)

A potential protective mechanism of high-intensity interval training against tetracycline-induced hepatic steatosis and testicular apoptosis in male Wistar rat: A crosstalk between the liver and testis

  • Masoumeh Ebadi Zahmatkesh,
  • Fatemeh Rostamkhani

DOI
https://doi.org/10.22122/jeoct.2023.432373.1101
Journal volume & issue
Vol. 3, no. 4
pp. 160 – 172

Abstract

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The presence of tetracycline in animal products has toxic and destructive effects on body tissues. In this study we investigate the potential protective mechanism of high-intensity interval training (HIIT) against tetracycline-induced hepatic steatosis (HS) and testicular apoptosis in male Wistar rat. In this study, forty-eight male Wistar rats (8-week, 220±10 gram) were randomly divaded into six groups of primary control (pre week one), primary HS (tetracycline-induced HS), secondary control (after week five), secondary HS, (5) HIIT, and HS+HIIT (after week five). Tetracycline was administered to rats 140 mg / kg for 7 days by gavage. HIIT was performed on rodent treadmill 5 days/week for 5 weeks. Oral exposure of tetracycline for 7 days caused severe testis damage as indicated by significant alterations in histomorphological, apoptosis, increase Bax, P53 and decease Bcl2 (gene and protein, p=0.001) compared to primary control. But the changes of PARP1 were not significant (p>0.05). However, HIIT and HS+HIIT groups significantly increased spermatogonium counts, spermatocyte cell counts & spermatid cell counts (p=0.001 for all) in line with Bcl-2 and PARP1 (gene and protein, p=0.001) and decreasing apoptotic cells, Bax and p53 compared with secondary HS group (p=0.001). This research provides the first evidence that the beneficial anti-apoptosis effects of HIIT on testis of rats poisoned with tetracycline. This beneficial effect of HIIT on hepatic steatosis and testicular damage and toxicity due to tetracycline might be mediated by inhibiting P53-induced BAX upregulation and preventing apoptosis-mediated degradation of PARP-1.

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