Target type: biologicalprocess
Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a carbon monoxide (CO) stimulus. [GOC:ecd]
Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that can be highly toxic. It is produced by the incomplete combustion of fossil fuels, and is also found in cigarette smoke. When inhaled, CO binds to hemoglobin in red blood cells with an affinity approximately 200 times greater than oxygen. This binding prevents oxygen from being transported to the body's tissues, leading to hypoxia, a condition of low oxygen levels.
The body's response to CO exposure involves several key mechanisms, including:
* **Hemoglobin binding:** As CO binds to hemoglobin, it forms carboxyhemoglobin (COHb), which disrupts the normal oxygen transport function of red blood cells. The severity of CO poisoning is directly related to the level of COHb in the blood.
* **Cellular respiration:** CO inhibits cellular respiration by interfering with the electron transport chain, which is crucial for ATP production. This disruption can lead to widespread cellular dysfunction and damage.
* **Cardiovascular effects:** CO can directly affect the cardiovascular system by inducing vasoconstriction, increasing heart rate, and decreasing cardiac output. These changes can lead to a reduction in blood flow to vital organs.
* **Neurological effects:** CO is known to be neurotoxic, causing a range of neurological symptoms including headache, dizziness, confusion, seizures, and coma. In severe cases, CO poisoning can lead to permanent brain damage.
* **Cellular defense mechanisms:** The body has certain defense mechanisms to counteract the effects of CO exposure. These include increased red blood cell production, increased ventilation rate, and the activation of antioxidant enzymes.
In addition to the direct effects of CO on the body, exposure to this gas can also trigger a number of secondary responses, such as:
* **Inflammation:** CO exposure can trigger inflammation, which can further exacerbate tissue damage and contribute to the progression of disease.
* **Immune system suppression:** CO can suppress the immune system, making the body more vulnerable to infections.
* **Oxidative stress:** CO can increase oxidative stress, which can lead to DNA damage and other cellular damage.
The response to CO exposure varies depending on the concentration of CO in the air, the duration of exposure, and the individual's susceptibility. Symptoms of CO poisoning can range from mild to severe, and in some cases, can be life-threatening. Early detection and treatment are crucial for reducing the risk of long-term complications.
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Protein | Definition | Taxonomy |
---|---|---|
Calcium-activated potassium channel subunit alpha-1 | A calcium-activated potassium channel subunit alpha-1 that is encoded in the genome of human. [PRO:WCB, UniProtKB:Q12791] | Homo sapiens (human) |
Interleukin-10 | An interleukin-10 that is encoded in the genome of human. [PRO:JAN, UniProtKB:P22301] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
ns 1619 | NS 1619 : A member of the class of benzimidazoles that is 1,3-dihydro-2H-benzimidazol-2-one in which the hydrogens at positions 1 and 5 are replaced are replaced by 2-hydroxy-5-(trifluoromethyl)phenyl and trifluoromethyl groups, respectively. It is an opener/activator of the large-conductance calcium-activated potassium channel (Bkca). NS 1619: structure given in first source | (trifluoromethyl)benzenes; benzimidazoles; phenols | potassium channel opener |
bms204352 | BMS204352: a calcium-sensitive opener of maxi-K potassium channels; structure in first source | ||
N-(5-chloro-2-hydroxyphenyl)-2-ethoxybenzamide | benzamides | ||
hg-9-91-01 | HG-9-91-01 : A member of the class of phenylureas that is a potent inhibitor of salt-inducible kinase 2, a potential target protein for therapy in ovarian cancer. HG-9-91-01: inhibits salt-inducible kinases; structure in first source | aminopyrimidine; dimethoxybenzene; N-alkylpiperazine; N-arylpiperazine; phenylureas; secondary amino compound | antineoplastic agent; salt-inducible kinase 2 inhibitor |