Protective role of 1α, 25-dihydroxyvitamin D3 against oxidative stress in nonmalignant human prostate epithelial cells

2008 ◽  
Vol 122 (12) ◽  
pp. 2699-2706 ◽  
Author(s):  
Bo-Ying Bao ◽  
Huei-Ju Ting ◽  
Jong-Wei Hsu ◽  
Yi-Fen Lee
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Protective Role ◽  
Human Prostate ◽  
Dihydroxyvitamin D3 ◽  
Prostate Epithelial Cells

scholarly journals Regulation of proliferation of prostate epithelial cells by 1,25-dihydroxyvitamin D3 is accompanied by an increase in insulin-like growth factor binding protein-3

2001 ◽  
Vol 170 (3) ◽  
pp. 609-618 ◽  
Author(s):  
CC Sprenger ◽  
A Peterson ◽  
R Lance ◽  
JL Ware ◽  
RH Drivdahl ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Human Prostate ◽  
Dihydroxyvitamin D3 ◽  
Prostate Epithelial Cell ◽  
Igf System ◽  
Prostate Epithelial Cells ◽  
Igf I ◽  
Igfbp 3

The biologically active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) has been shown to regulate the proliferation of human prostate epithelial cell lines. Since the insulin-like growth factor (IGF) system is involved in the transformation process of epithelial cells, the following study was undertaken to determine if the IGF system, in particular IGF binding protein-3 (IGFBP-3), is altered by 1,25-(OH)2D3 in normal prostate epithelial cells as part of a mechanism for inhibition of transformation. Two cell systems were used in this study: (1) primary cultures of benign human prostate epithelial cells (PECs) and (2) an SV40-T immortalized prostate epithelial cell line (P153) that is non-tumorigenic. 1,25-(OH)2D3 was added to parallel sets of PECs and P153 cells in addition to the presence or absence of IGF-I or des(1-3)IGF-I. Treatment with 1,25-(OH)2D3 resulted in significant growth inhibition of both PECs and P153 cells. Furthermore, 1,25-(OH)2D3 inhibited IGF-induced proliferation, but this was partially reversed by high concentrations of IGF-I. Western ligand blots of condition media demonstrated a significant increase in IGFBP-3; likewise Northern blots demonstrated an increase in mRNA for IGFBP-3. Proliferation assays using an antibody designed to block the IGF-independent effects of IGFBP-3 failed to reverse the inhibitory effect of 1,25-(OH)2D3. Thus, IGFBP-3 acts in an IGF-dependent manner to inhibit cell growth of benign prostate epithelial cells.

Role of connexin 43 in cadmium-induced proliferation of human prostate epithelial cells

2017 ◽  
Vol 37 (8) ◽  
pp. 933-942 ◽  
Author(s):  
Qingping Liu ◽  
Xiaoli Ji ◽  
Zehe Ge ◽  
Haipeng Diao ◽  
Xiuli Chang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Connexin 43 ◽  
Human Prostate ◽  
Prostate Epithelial Cells

Estrogen receptor β plays a protective role in zearalenone-induced oxidative stress in normal prostate epithelial cells

2019 ◽  
Vol 172 ◽  
pp. 504-513 ◽  
Author(s):  
Karolina Kowalska ◽  
Dominika Ewa Habrowska-Górczyńska ◽  
Kinga Anna Urbanek ◽  
Kamila Domińska ◽  
Agata Sakowicz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Protective Role ◽  
Estrogen Receptor Β ◽  
Normal Prostate ◽  
Prostate Epithelial Cells

scholarly journals Protective Role of Glutathione in the Hippocampus after Brain Ischemia

2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Excitatory Amino Acid ◽  
Ischemia Reperfusion ◽  
Thiol Group ◽  
Protective Role ◽  
Key Factor ◽  
Rate Limiting ◽  
Cysteine Uptake

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.

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