Adaptation to Intermittent Hypoxia and its use for Protecting the Heart from Stress and Ischemic Damage
Felix Z. Meerson in Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
This chapter demonstrates first experimentally and then clinically, that adaptation to moderate, rationally dosed hypoxia can be used to protect the heart against stress-induced and ischemic damage. Such a broad structural basis of adaptation to hypoxia should not be surprising, since in the whole organism hypoxia may arise not only from reduced oxygen content in the inhaled air and is not an exclusive domain of pathology. On the contrary, in the healthy organism hypoxemia or relative tissue hypoxia inevitably and most commonly occurs in significant loads on the whole organism or on particular organs and systems. Since adaptation to intermittent hypoxia activates the central stress-limiting systems and concurrently restricts or abolishes the disturbances to cardiac electric stability, it was reasonable to assess its effect on the course of neurasthenia and mentioned arrhythmias. After adaptation to intermittent hypoxia, the patients’ condition improved and the high erythrocyte sedimentation rate was attenuated.
Hypoxia and Angiogenesis
Loredana G. Marcu, Iuliana Toma-Dasu, Alexandru Dasu, Claes Mercke in Radiotherapy and Clinical Radiobiology of Head and Neck Cancer, 2018
Tumour hypoxia is known as one of the major factors that influence the response of head and neck cancer (HNC) to treatment in general and to radiotherapy in particular. Hypoxia occurs in tumours because of the particular characteristics of the tumour vasculature leading to impaired oxygenation of the cells. Radiobiological hypoxia, defined as the lack of oxygen in the cellular tumour microenvironment, has been recognised for a long time as one of the critical factors that determine the cellular response to radiation. Hypoxic cells can also acquire a mutator phenotype leading to decreased DNA repair, increased chromosomal instability as well as an increased mutation rate. Molecular factors might further elucidate the differences between acute and chronic hypoxia observed in solid tumours including HNC. A special class of methods for identifying hypoxia in HNC is based on the expression of endogenous molecular markers of cellular hypoxia, such as hypoxia-inducible factor 1 (HIF-1).
Environmental Hypoxia
Alan G. Heath in Water Pollution and Fish Physiology, 2018
This chapter presents the physiological responses of fish to hypoxia or anoxia. Hypoxia refers to any condition in which the amount of oxygen is measurably below air saturation levels. The chapter provides the process of respiratory gas exchange and transport during hypoxia to the biochemical changes involved in anaerobic metabolism during anoxia. There are several potential causes of environmental hypoxia, some of which are not due to human activities. Some species of freshwater fish are extremely resistant to low levels of oxygen, or even anoxia. Within the gill, if transport of oxygen by the blood is compromised by some chemicals such as nitrate, there is a reduced ability to tolerate hypoxia. The main reason for adjusting the various processes involved in taking up oxygen from the water is to increase respiratory independence (or regulation). Acclimation to hypoxia would seem to be a very important ability for those fish that experience chronic conditions of low oxygen.
Panax ginseng increases hypoxia-induced down-regulated cellular response related genes in human neuroblastoma cells, SK–N–MC
Published in Neurological Research, 2007
Haejeong Park, HakJae Kim, Eunyoung Ha, SeoHyun Yoon, Mi-Ja Kim, MeeSuk Hong, Kang-Hyun Leem, Seung-Jae Hong, JongSoo Yang, Joo-Ho Chung
Background: Many studies have suggested that hypoxia plays a crucial role in the pathogenesis of various neurological disorders. To determine protective effect of Panax ginseng (PG) on hypoxia (0.1% O2)-induced cell death in human neuroblastoma cells SK–N–MC, we profiled the gene expression among hypoxia, PG-treated hypoxia and normoxia groups. Methods: To determine protective effect on hypoxia-induced cytotoxicity of PG, we performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. We compared the gene expression profiles among hypoxia, PG-treated hypoxia (100 μg/ml, 6 hours) and normoxia groups using 8K human cDNA microarray analysis. Additionally, in order to identify differentially expressed genes between hypoxia and PG-treated hypoxia groups, hierarchical clustering of genes was also performed. Results: MTT assay showed that PG protected hypoxia-induced cell death. In cDNA microarray analysis, hypoxia remarkably down-regulated IGF-II mRNA-binding protein 3 (IMP-3), integrin alpha 2 (ITGA2), syndecan binding protein (SDCBP), insulin-like growth factor binding protein 3 (IGBP3) and M-phase phosphoprotein 10 (MPHOSPH10), belonging to category of cellular physiologic response (global M
Hypoxia: A Double-Edged Sword in Cancer Therapy
Published in Cancer Investigation, 2016
Hamed Manoochehri Khoshinani, Saeid Afshar, Rezvan Najafi
ABSTRACT Hypoxia is a common feature of malignant tumors. There is an interactive connection between hypoxia and chemoresistance, radioresistance, invasiveness, and angiogenesis. Therefore, tumor hypoxia has been considered as a validated target for treating cancer. This review focuses on the role of hypoxia on chemoresistance and radioresistance. In addition, we address several approaches targeting tumor hypoxia, known as hypoxia-targeted therapy.
Hypoxia and hypoxia mimetics differentially modulate histone post-translational modifications
Published in Epigenetics, 2021
Kuo-Feng Hsu, Sarah E. Wilkins, Richard J. Hopkinson, Rok Sekirnik, Emily Flashman, Akane Kawamura, James S.O. McCullagh, Louise J. Walport, Christopher J. Schofield
ABSTRACT Post-translational modifications (PTMs) to the tails of the core histone proteins are critically involved in epigenetic regulation. Hypoxia affects histone modifications by altering the activities of histone-modifying enzymes and the levels of hypoxia-inducible factor (HIF) isoforms. Synthetic hypoxia mimetics promote a similar response, but how accurately the hypoxia mimetics replicate the effects of limited oxygen availability on the levels of histone PTMs is uncertain. Here we report studies on the profiling of the global changes to PTMs on intact histones in response to hypoxia/hypoxia-related stresses using liquid chromatography-mass spectrometry (LC-MS). We demonstrate that intact protein LC-MS profiling is a relatively simple and robust method for investigating potential effects of drugs on histone modifications. The results provide insights into the profiles of PTMs associated with hypoxia and inform on the extent to which hypoxia and hypoxia mimetics cause similar changes to histones. These findings imply chemically-induced hypoxia does not completely replicate the substantial effects of physiological hypoxia on histone PTMs, highlighting that caution should be used in interpreting data from their use.