Concentration-Dependent Effects of Zinc Sulfate on DU-145 Human Prostate Cancer Cell Line: Oxidative, Apoptotic, Inflammatory, and Morphological Analyzes

Hacioglu C., Kaçar S., Kar F., Kanbak G., Şahintürk V.

BIOLOGICAL TRACE ELEMENT RESEARCH, vol.195, no.2, pp.436-444, 2020 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 195 Issue: 2
  • Publication Date: 2020
  • Doi Number: 10.1007/s12011-019-01879-0
  • Journal Name: BIOLOGICAL TRACE ELEMENT RESEARCH
  • Journal Indexes: 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
  • Page Numbers: pp.436-444
  • Keywords: Zinc sulfate, DU-145 prostate cancer cells, Oxidative stress, Apoptosis, Inflammation, TNF-ALPHA, SURVIVAL, STRESS, GROWTH, HYPERPLASIA, INHIBITION, DEFICIENCY, METABOLISM, ASSAY, IL-6
  • Kütahya Health Sciences University Affiliated: Yes

Abstract

Zinc takes part in several of cellular signaling pathways, containing defense against free radicals, apoptosis, and inflammation. However, interaction between zinc and prostate cancer progression is poorly understood. Therefore, zinc treatment in DU-145 human prostate cancer cells was investigated. First, zinc sulfate (ZnSO4) concentrations with antiproliferative effect were determined using MTT assay. Then, ZnSO4-induced oxidative damage was evaluated by malondialdehyde (MDA) levels, glutathione (GSH) levels, total oxidant status (TOS) levels, and total antioxidant status (TAS) levels. Apoptotic effects of ZnSO4 were determined by measuring biochemical and immunohistochemical parameters including caspase 3 (CASP3), cytochrome C (CYC), Bcl-2-associated X protein (Bax), and B cell CLL/lymphoma 2 (Bcl-2) levels. Inflammatory effects of ZnSO4 were investigated by measuring interleukin-6 (IL-6) levels and tumor necrosis factor-alpha (TNF-alpha) levels. Finally, morphological analysis was performed using hematoxylin-eosin staining. We found that ZnSO4 caused a concentration-dependent increase in oxidative stress, apoptosis, and inflammation pathways. Moreover, there were a number of morphological alterations in treated cells depending on the ZnSO4 concentration. Consequently, our data showed that zinc acts as a regulator of increased oxidative damage and apoptosis through the upregulation of TNF-alpha and IL-6.