Boron, a Trace Mineral, Alleviates Gentamicin-Induced Nephrotoxicity in Rats


Ince S., Kucukkurt I., Demirel H. H., Arslan-Acaroz D., Varol N.

BIOLOGICAL TRACE ELEMENT RESEARCH, cilt.195, sa.2, ss.515-524, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 195 Sayı: 2
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1007/s12011-019-01875-4
  • Dergi Adı: BIOLOGICAL TRACE ELEMENT RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Agricultural & Environmental Science Database, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Food Science & Technology Abstracts, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Sayfa Sayıları: ss.515-524
  • Anahtar Kelimeler: Boron, Gentamicin, Oxidative stress, Nephrotoxicity, Inflammation, INDUCED OXIDATIVE STRESS, GREEN TEA EXTRACT, PROTECTIVE ROLE, KIDNEY INJURY, BLOOD-CELLS, INFLAMMATION, THYMOQUINONE, DYSFUNCTION, EXPRESSION, INHIBITOR
  • Gazi Üniversitesi Adresli: Evet

Özet

The present study was considered to assess the protective effects of boron (B) on gentamicin-induced oxidative stress, proinflammatory cytokines, and histopathological changes in rat kidneys. Rats were split into eight equal groups which were as follows: control (fed with low-boron diet); gentamicin group (100 mg/kg, i.p.); B-5, B-10, and B-20 (5, 10, and 20 mg/kg B, i.p.) groups; gentamicin (100 mg/kg, i.p.) plus B-5, B-10, and B-20 (5, 10, and 20 mg/kg B, i.p.) groups. B was given to rats 4 days before the gentamicin treatment and B administration was completed on the 14th day. Gentamicin administration was started on the 4th day and finished on the 12th day. Gentamicin increased malondialdehyde levels, while reduced glutathione levels in the blood and kidney. Furthermore, superoxide dismutase and catalase activities of erythrocyte were decreased. Besides, serum and kidney nitric oxide and 8-dihydroxyguanidine levels were increased by gentamicin. Additionally, serum levels and kidney mRNA expressions of TNF-alpha, NF kappa B, IL-1 beta, and IFN-gamma were found to be the highest in the gentamicin group. Histopathologically, interstitial hemorrhage and tubular necrosis were detected in the kidneys of the gentamicin group. Nonetheless, B administration reversed gentamicin-induced lipid peroxidation, antioxidant status, and inflammation. In conclusion, B has a preventive effect against gentamicin-induced nephrotoxicity and ameliorates kidney tissues of the rat.