ArticleCell stress & chaperones2009
Heat-shock response protects peripheral blood mononuclear cells (PBMCs) from hydrogen peroxide-induced mitochondrial disturbance.
Article in Cell stress & chaperones, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Astaxanthin supplementation in Arabian racing horses mitigates oxidative stress and inflammation in peripheral blood mononuclear cells through enhanced mitophagy.Scientific reports · 2025Article
- Erythropoietin inhibits ferroptosis and ameliorates neurological function after spinal cord injury.Neural regeneration research · 2023Article
- Flavokawains A and B from kava (Piper methysticum) activate heat shock and antioxidant responses and protect against hydrogen peroxide-induced cell death in HepG2 hepatocytes.Pharmaceutical biology · 2016Article
- Genetic Polymorphisms of X-ray Repair Cross-Complementing Group 1 and Apurinic/Apyrimidinic Endonuclease-1 in Chronic Obstructive Pulmonary Disease.Inflammation · 2016Article
- Can Melatonin Act as an Antioxidant in Hydrogen Peroxide-Induced Oxidative Stress Model in Human Peripheral Blood Mononuclear Cells?Biochemistry research international · 2016Article
- Genetic polymorphisms of HSP70 in age-related cataract.Cell stress & chaperones · 2013Article
- Astaxanthin ameliorates heat stress-induced impairment of blastocyst development in vitro:--astaxanthin colocalization with and action on mitochondria--.Journal of assisted reproduction and genetics · 2013Article
- Heat Shock Protein 70 Expression is Increased in the Liver of Neonatal Intrauterine Growth Retardation Piglets.Asian-Australasian journal of animal sciences · 2012Article
- Functional polymorphisms in XRCC-1 and APE-1 contribute to increased apoptosis and risk of ulcerative colitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012Article
- Impaired glycolytic response in peripheral blood mononuclear cells of first-onset antipsychotic-naive schizophrenia patients.Molecular psychiatry · 2011Article
- The Hsp72 response in peri-parturient dairy cows: relationships with metabolic and immunological parameters.Cell stress & chaperones · 2010Article
- Modulation of cytotoxic and genotoxic effects of nanoparticles in cancer cells by external magnetic field.Cancer nanotechnologyArticle
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was designed to investigate ex vivo the protective mechanisms of heat-shock response against H(2)O(2)-induced oxidative stress in peripheral blood mononuclear cells (PBMCs) of rats. Twenty-four hours later, heat-shock treatment was executed in vivo; rat PBMCs were collected and treated with H(2)O(2). The accumulation of reactive oxygen species and the mitochondrial membrane potential were evaluated by intracellular fluorescent dHE and JC-1 dye staining, respectively, and expression of HSP72 and cytochrome c was detected by Western blot analysis. Cellular apoptosis was assayed by TUNEL staining and double staining of Annexin V and PI. The results showed that H(2)O(2)-induced oxidative stress leads to intracellular superoxide accumulation and collapse of the mitochondrial membrane potential in rat PBMCs. Moreover, cellular apoptosis was detected after H(2)O(2) treatment, and the release of mitochondrial cytochrome c from mitochondria to cytosol was significantly enhanced. Heat-shock pretreatment decreases the accumulation of intracellular superoxide in PBMCs during H(2)O(2)-induced oxidative stress. Moreover, heat-shock treatment prevents the collapse of the mitochondrial membrane potential and cytochrome c release from mitochondria during H(2)O(2)-induced oxidative stress. In conclusion, mitochondria are critical organelles of the protective effects of heat-shock treatment. Cellular apoptosis during H(2)O(2)-induced oxidative stress is decreased by heat-shock treatment through a decrease in superoxide induction and preservation of the mitochondrial membrane potential.
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