Effects of sinapic acid on lead acetate-induced oxidative stress, apoptosis and inflammation in testicular tissue

Creative Commons License

Tuncer S. Ç., Akarsu S. A., Küçükler S., Gür C., Kandemir F. M.

ENVIRONMENTAL TOXICOLOGY, cilt.38, sa.11, ss.2656-2667, 2023 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 38 Sayı: 11
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1002/tox.23900
  • Dergi Adı: ENVIRONMENTAL TOXICOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, Chimica, Compendex, EMBASE, Environment Index, Food Science & Technology Abstracts, Geobase, Greenfile, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Sayfa Sayıları: ss.2656-2667
  • Anahtar Kelimeler: apoptosis, inflammation, lead acetate, oxidative stress, sinapic acid, EXPOSURE, EXPRESSION, DAMAGE, RATS, NEPHROTOXICITY, CASPASE-3, QUALITY
  • Atatürk Üniversitesi Adresli: Evet

Özet

In this study, the effect of lead acetate (PbAc) and sinapic acid (SNP) administration on oxidative stress, apoptosis, inflammation, sperm quality and histopathology in testicular tissue of rats was tried to be determined. PbAc was administered at a dose of 30 mg/kg/bw for 7 days to induce testicular toxicity in rats. Oral doses of 5 and 10 mg/kg/bw SNP were administered to rats for 7 days after PbAc administration. According to our findings, while PbAc administration increased MDA content in rats, it decreased GPx, SOD, CAT activity and GSH content. NF-kB, IL-1 & beta;, TNF-& alpha;, and COX-2, which are among the inflammation parameters that increased due to PbAc, decreased with the administration of SNP. Nrf2, HO-1, and NQO1 mRNA transcript levels decreased with PbAc, but SNP treatments increased these mRNA levels in a dose-dependent manner. RAGE and NLRP3 gene expression were upregulated in PbAc treated rats. MAPK14, MAPK15, and JNK relative mRNA levels decreased with SNP treatment in PbAc treated rats. While the levels of apoptosis markers Bax, Caspase-3, and Apaf-1 increased in rats treated with PbAc, the level of Bcl-2 decreased, but SNP inhibited this apoptosis markers. PbAc caused histopathological deterioration in testis tissue and negatively affected spermatogenesis. When the sperm quality was examined, the decrease in sperm motility and spermatozoon density caused by PbAc, and the increase in the ratio of dead and abnormal spermatozoa were inhibited by SNP. As a result, while PbAc increased apoptosis and inflammation by inducing oxidative stress in testicles, SNP treatment inhibited these changes and increased sperm quality.