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Related Concept Videos

Hypoxia01:23

Hypoxia

Hypoxia is a medical condition characterized by an inadequate oxygen supply to body tissues. It typically manifests as a bluish discoloration of the skin and mucosae, especially in fair-skinned individuals, when hemoglobin (Hb) saturation drops below 75%.
Types of Hypoxia
There are four primary types of hypoxia, each resulting from a different cause:
1. Anemic hypoxia: This type occurs due to insufficient oxygen delivery caused by a lack of red blood cells (RBCs) or RBCs with abnormal or...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Oxygen Requirements and Growth Patterns01:29

Oxygen Requirements and Growth Patterns

Microorganisms exhibit diverse oxygen requirements and growth patterns driven by their metabolic strategies and environmental adaptations. Oxygen, while essential for many organisms, can also be toxic under certain conditions, shaping how microorganisms grow and survive.Oxygen Requirements of MicroorganismsMicroorganisms are classified based on their ability to use or tolerate oxygen:● Obligate aerobes like Mycobacterium tuberculosis need oxygen for energy production, as it serves as the...
Oxygen Transport in the Blood01:27

Oxygen Transport in the Blood

Hemoglobin (Hb) is a crucial molecule in the human body, consisting of four polypeptide chains, each bound to an iron-containing heme group. This unique structure enables hemoglobin to bind to oxygen, with each molecule capable of combining with four molecules of oxygen, leading to rapid and reversible oxygen loading. When fully loaded with oxygen, it is called oxyhemoglobin, while hemoglobin that has released oxygen is called reduced hemoglobin or deoxyhemoglobin. As hemoglobin binds oxygen,...
Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:

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Related Experiment Video

Updated: Jul 7, 2026

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice
09:13

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice

Published on: July 11, 2025

Hyperoxia causes maturation-dependent cell death in the developing white matter.

Bettina Gerstner1, Tara M DeSilva, Kerstin Genz

  • 1Department of Neurology and the F. M. Kirby Neurobiology Center, Children's Hospital Boston, Boston, Massachusetts 02115, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|February 1, 2008
PubMed
Summary
This summary is machine-generated.

High oxygen exposure causes oxidative stress and triggers apoptosis in developing oligodendrocytes (OLs), leading to white matter injury in neonatal rats. This suggests a potential mechanism for brain damage in premature infants.

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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

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Last Updated: Jul 7, 2026

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice
09:13

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice

Published on: July 11, 2025

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Neonatal Medicine

Background:

  • Periventricular leukomalacia is a primary cause of cerebral palsy in preterm infants.
  • Oxygen exposure is a potential contributing factor to brain injury in vulnerable preterm neonates.
  • Oligodendrocytes (OLs) are crucial for myelin formation and are susceptible to injury.

Purpose of the Study:

  • To investigate the mechanisms of maturation-dependent oligodendrocyte death induced by hyperoxia.
  • To determine the role of oxidative stress and apoptosis in hyperoxia-induced white matter injury.
  • To assess the relevance of these findings to neonatal brain injury in premature infants.

Main Methods:

  • In vitro: Exposure of developing and mature OLs to 80% oxygen, assessed by LDH assay.
  • In vivo: Exposure of neonatal rat pups (postnatal days 3, 6, 10) to 80% oxygen, followed by myelin basic protein (MBP) staining.
  • Investigated caspase-dependent apoptosis, BCL2 overexpression, reactive oxygen species (ROS) generation, and lipoxygenase/superoxide dismutase activity.

Main Results:

  • Hyperoxia induced significant cell death in developing OLs (pre-OLs) via caspase-dependent apoptosis, but not in mature OLs.
  • Oxidative stress, including superoxide and ROS generation, was detected early in oxygen-exposed pre-OLs.
  • In vivo, hyperoxia reduced MBP expression in P3 and P6 rat pups, indicating white matter injury, but not in P10 pups.

Conclusions:

  • Hyperoxia triggers maturation-dependent apoptosis in pre-OLs through oxidative stress and caspase activation.
  • This process leads to white matter injury in the neonatal rat brain, mirroring findings in preterm infants.
  • Targeting oxidative stress and apoptotic pathways may offer neuroprotective strategies for premature infants.