To learn the basics of eicosanoids:
Meet the eicosanoid families
Or ... Go straight to the eicosanoid chart
• The PROSTAGLANDIN family (a prostanoid): Produced in most cells;
Series 1 (PGE1) and Series 3 prostaglandins. Counter inflammation
Series 2 prostaglandins. Significant ones are PGD2, PGE2, PGF2α;, PGI2 (a.k.a. prostacyclin. a potent vasodilator produced mainly by endothelial cells, which comprise the inner lining of blood and lymphatic vessels, and epithelial cells lining the inside of other hollow organs e.g. bronchial epithelial cells in airways, and the skin's epidermis.
• The THROMBOXANE family (a prostanoid): Produced mainly in platelets, also placenta, lungs;
Mainly thromboxane TXA2. Promotes blood clotting /platelet-aggregation and is a potent vasoconstrictor. Also broncho-constrictive.
• The LEUKOTRIENE family: Produced in leukocytes. i.e. white blood cells: Series 4 and Series 5 leukotrienes
• The EOXIN family: Produced in immune system eosinophils (white blood cells), mast cells, and some other tissues. Generally steps up inflammatory response.
• The LIPOXIN and RESOLVIN families: Deal with reducing excessive tissue injury and the resolution of inflammation.
LIPOXINS ( Produced in platelets, neutrophils, red blood cells and reticulocytes; also by low dose aspirin).
RESOLVINS (Produced in most cells) Potent anti-inflammatory agents that as their name suggests, resolve inflammation. They limit the extent of inflammation by blocking the actions of inflammatory prostanoids (prostaglandins and thromboxanes) and also clear away breakdown products of inflammation process. E.g. RVD1-6
• The PROTECTIN family
Eicosanoid activity can not be differentiated as "good" and "bad"
If you've been injured, promoting inflammation is very necessary to aid repair, but can be overly painful and damage tissue if done to excess. Causing the blood to clot can be life-saving if you just cut yourself, but can cause a heart attack if overdone in the arteries, and lastly, cell-proliferation is needed to repair tissue, but when out of control can cause a tumor. Excessive or unresolved inflammation, or overreaction to stimuli can lead to uncontrolled tissue damage and health problems.
Eicosanoid activity is complex
The eicosanoid families, PROSTAGLANDINS, THROMBOXANES, LEUKOTRIENES, EOXINS, LIPOXINS and RESOLVINS have family members with specific functions. However, their activity can be confusing, since their tissue location, and which enzyme produced them can sometimes determine whether they either promote or resolve inflammation, .
Dietary omega-3 EPA and omega-6 GLA counter the predominately inflammatory effects of omega-6 AA in three ways:
• Competitive inhibition. DGLA and EPA compete with AA for COX and LOX enzymes, such that the presence of DGLA and also EPA in tissues lowers the production of AA's eicosanoids
• Displacement. Increased dietary omega-3 results in decreased AA in brain and other tissue. Green et al, 2005
• Direct counteraction. Some DGLA and EPA-derived eicosanoids counteract their AA derived counterparts. E.g. PGE1 derived from DGLA acts against PGE2 derived from AA.
COX enzymes
COX-1 - "The housekeeper"
COX-1 is expressed constitutively in most tissues and regulates basal levels of prostaglandins to maintain general homeostasis. Only COX-1 produces PROSTAGLANDINS that protect the stomach and intestinal lining
COX-1 is also actively involved in certain traumatic/stimulated events. Only COX-1 produces prostaglandins that activate platelets and constrict airways.
The human COX-1 gene is located on chromosome 9
COX-2 - "The main activator"
COX-2 enzyme is mostly induced in "times of trouble". Responsible for releasing PROSTAGLANDINS after an infection, injury, or in cancer development, COX-2 expression is induced by the cytokines interleukin (IL)-1, IL-2, and TNF, as well as by lipopolysaccharide (LPS) produced by Gram-negative bacteria. Kang et al, 2007
COX-2 enzyme inhibitors reduce the prostanoids PGI2, PGD2, PGE2 PGF2α;, and thromboxane A2
The human COX-2 gene is located on chromosome 1
Traditional NSAIDs (e.g. aspirin, Aleve, Motrin) suppress both COX-1 and COX-2 enzymes
NSAIDS (Cox enzyme inhibitors / Coxibs) - Anti-inflammatory drugs WARNING!
"Orange" represents activity altering the status quo, some increasing inflammation.
"Turqoise" represents more of a "calming down" / going-back-to-normal action and/or resolving the inflammation.
"Red" represents eicosonoids having an inflammatory effect
This chart is anything but simple! - however, it attempts to describe the competition between consumed omega-3 and omega-6 fats for the enzymes which convert omega-3 fatty acids to calming eicosanoids and/or convert omega-6 fats to mostly active eicosanoids.
Effects of the calming eicosanoids produced from omega-3 fats (and some omega-6 fats when omega-3 is present) are:
• Anti-inflammatory / reducing pain;
• Relaxing smooth muscles (dilating blood vessels in the circulatory system and bronchial airways, relaxing walls of stomach, lung, intestine, bladder, uterus, other hollow organs;
• Protecting stomach lining (gastric mucosa);
• Controlling cell multiplication (proliferation);
• Normalizing immune system, inhibiting blood clot formation, promoting sleep, preventing inhibition of hair growth, .
Effects of the active eicosanoids produced mostly from omega-6 fats are: Basically, the opposite of those produced by omega-3.
• Inflammation / pain;
• Constriction of blood vessels / Contracting bronchial airways, and other hollow organ walls;
• Promoting blood clots;
• immune system stimulation;
• Cell proliferation (cancer is cells multiplying out of control).
Both omega-6's active effects and omega-3's calming effects are necessary IN BALANCE. However, we consume much greater amounts of omega-6 than necessary, and little to no omega-3. See the problem?
Prostanoids: Prostaglandins & Thromboxanes(produced in most cells via enzymes COX-1 (housekeeping) and COX-2 (mostly induced under stress conditions) |
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PGE1 |
Directly derived from: Omega-6 DGLA in breast milk. via COX enzymes. | ||
Indirectly derived
from: Omega-6 LA in nuts, seeds,
vegetable oils, or legumes or GLA
in borage, evening primrose or blackcurrant oil,
which can all ultimately be converted to
Omega-6 AA, and then to
more
inflammatory /active eicosanoids
PG2, TX2, LT4.
and
EX4. However -
this
omega-6 AA
pathway leading to more inflammatory eicosanoids
competes with
omega-3
presence
for Δ5D, Δ6D
and COX enzymes
that prefer pathways to the more calming,
anti-inflammatory
PG1 (incl.
PGE1), TX1, PG3, TX3 and
LT5 series of eicosanoids. Sufficient omega-3 SDA (in blackcurrant / wild seed oil or derived from omega-3 ALA foods) must be present to ensure COX enzyme conversion of Omega-6 DGLA to anti-inflammatory PG1 series (incl. PGE1) by competing for Δ5D enzymes, instead of COX conversion to Omega-6 AA and then the more active eicosanoids. "EFA Conversion Chart" provides a visual aid to understanding these complicated, interacting conversion pathways. |
|||
P G E 1 |
ALL CELLS
|
![]() Anti-inflammatory |
![]() |
Sesame lignans promote conversion of omega-6 DGLA to anti-inflammatory PGE1 in favor of pro-inflammatory omega-6 AA | |||
Inhibit cell proliferation |
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P G E 1 |
BLOOD / LYMPH VESSELS |
![]() Vasodilator |
|
P G E 1 |
PLATELETS |
Image: deaggregation | |
Inhibits platelet aggregation; data suggests via promotion of Prostacyclin receptor (IP) Nie et al, 2020 | |||
P G E 1 |
IMMUNE SYSTEM CELLS |
![]() |
|
TUMORS | |||
Inhibit cell proflieration | |||
P G E 1 |
BRONCHIAL AIRWAYS |
![]() |
|
PGD2 |
Directly derived from: Omega-6 AA in meat and eggs. If present, Omega-3 EPA competes for COX-1 or COX-2 enzymes reducing their conversion of Omega-6 AA to PGD2 and other inflammatory /active eicosanoids: PG2, TX2,, LT4. and EX4. | ||
Indirectly derived
from: Omega-6 LA in nuts, seeds,
vegetable oils, or legumes, or Omega-6 DGLA
in breast milk, or GLA
in borage, evening primrose or blackcurrant oil,
which can all ultimately be converted to
Omega-6 AA, and then to
inflammatory /active eicosanoids:
PG2
(incl. PGD2), TX2, LT4.
and
EX4 via COX enzymes.. However -
this
omega-6 AA
pathway leading to more inflammatory eicosanoids
competes with
omega-3
presence
for Δ5D, Δ6D
and COX enzymes
that prefer pathways to the more calming,
anti-inflammatory
PG1 (incl.
PGE1), TX1, PG3, TX3 and
LT5 series of eicosanoids. "EFA Conversion Chart" provides a visual aid to understanding these complicated, interacting conversion pathways. |
|||
P G D 2 |
AIRWAYS; |
![]() |
|
Released by I.S. Mast cells - Involved in allergic rhinitis and allergic bronchial asthma. Attracts neutrophils (WBCs that fight infection and heal injuries). Involved in late phase reactions to allergens (6 hrs after exposure). PGD2 has 10 times higher concentration in asthma patients compared to control patients. | |||
P G D 2 |
PULMONARY PLACENTAL VESSELS |
![]() |
|
Released by I.S. Mast cells - PGD2 is a potent vasoconstrictor via thromboxane/endoperoxide (TX/E) receptor activation in pulmonary vessels, but this mechanism is not responsible for vasoconstriction in systemic vessels or in airway. King, 1991 | |||
P G D 2 |
BLOOD / LYMPH VESSELS |
![]() |
![]() |
PubMed | |||
P G D 2 |
PLATELETS
|
Image: platelet deaggregation | |
Platelet activation inhibitor- reduces platelet aggregation (blood clotting) | |||
P G D 2 |
UTERINE blood vessels | ![]() |
|
Released by Mast Cells - PGD2 can promote mild vasodilation if TX/E is blocked. King, 1991 PGD2 dilates uterine blood vessels. Together with its ability to constrict placental blood vessels, it may control utero-placental blood flow. | |||
P G D 2 |
Mast cells in BRAIN |
||
Most abundant prostanoid in mammalian brain; PGD2 promotes sleep [ Encyclopedia of Sleep, 2013] | |||
P G D 2 |
Mast cells in SKIN
|
![]() |
|
PGD2 is the primary mediator of vasodilation after taking niacin (vitamin B3) - the so-called "niacin flush". Involved in urticuria (hives), and balding- a causal link was found between elevated levels of localized PGD2 and hair growth inhibition (byincreasing Prostaglandin D2 synthase). Garza et al, 2012. | |||
PGE2/PGE2
|
Directly derived from: Omega-6 AA in meat and eggs. If present, Omega-3 EPA competes for COX-1 or COX-2 enzymes reducing their conversion of Omega-6 AA to PGD2 and other inflammatory /active eicosanoids: PG2, TX2,, LT4. and EX4. | ||
Indirectly derived
from: Omega-6 LA in nuts, seeds,
vegetable oils, or legumes, or Omega-6 DGLA
in breast milk, or GLA
in borage, evening primrose or blackcurrant oil,
which can all ultimately be converted to
Omega-6 AA, and then to
inflammatory /active eicosanoids:
PG2, TX2, LT4.
and
EX4 via COX enzymes.. However -
this
omega-6 AA
pathway leading to more inflammatory eicosanoids
competes with
omega-3
presence
for Δ5D, Δ6D
and COX enzymes
that prefer pathways to the more calming,
anti-inflammatory
PG1 (incl.
PGE1), TX1, PG3, TX3 and
LT5 series of eicosanoids. "EFA Conversion Chart" provides a visual aid to understanding these complicated, interacting conversion pathways. |
|||
P G E 2 |
BRAIN; JOINTS |
![]() |
|
Via Cox-2 - Promotes all signs of classic inflammation: i.e. redness, swelling and pain. Redness and edema result from increased blood flow into the inflamed tissue through PGE2-mediated increase in arterial dilation and microvascular permeability. Pain results from the action of PGE2 on peripheral sensory neurons and on central sites within the spinal cord and the brain Quercetin reduces PGE2 in RA joints Link |
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P G E 2 |
TUMORS Cell proliferation |
Image cell proliferation | |
Promotes tumor growth: PGE2 is the most abundant prostaglandin found in various human malignancies, including colon, lung, breast, and head and neck cancer, also often associated with a poor prognosis. In contrast, the enzyme that catalyzes the degradation of PGE2 (15-PGDH, an antagonist /suppressor of Cox-2) is highly expressed in normal tissues but is ubiquitously lacking in human colon, gastric, lung and breast cancer resulting in increased endogenous PGE2 levels in these tumors. Furthermore, there may be a negative feedback loop, since a product of the Cox-2 enzymatic pathway, upregulates the expression of 15-PGDH in breast cancer MDA-MD-231 cells. 15-PGDH is being investigated as a potential avenue for tissue regeneration. PubMed. Prostaglandin E Synthase (PGES) converts PGH to PGE | |||
P G E 2 |
Walls of: BLOOD / LYMPH VESSELS. STOMACH, INTESTINE, BLADDER, UTERUS
|
![]() ![]() |
![]() |
Dilates blood vessels in kidneys
PubMed Relaxes Vascular SMCs which form the supporting tissue of arteries, veins, capillaries & lymphatic vessels) and SMCs in walls of other hollow organs: stomach, intestine, bladder, uterus, others |
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STOMACH /INTESTINAL MUCOSA |
Image gastric mucosa | ||
P G E 2 |
Via Cox1 - Protects stomach
and intestinal lining; Gastric mucosa: ↑ mucous /bicarbonate secretion; ↑ mucosa blood flow; ↓ gastric acid /PEPSIN secretion; Intestinal mucosa: ↑ duodenal mucus secretion Provides gastrointestinal integrity (via Cox-2?) |
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FERTILITY | |||
Regulates immune responses; Involved in fertility | |||
UTERUS | |||
Dinoprostone (PGE2) is an FDA approved drug for evacuating the uterus (i.e. promoting abortion or inducing labor; helps dilate cervix and uterine wall (myometrium). However, PGE2 may also downregulate processes that contribute to the onset of human labour and may be beneficial in helping to maintain pregnancy towards term. Molecular Human Reproduction Article | |||
P G E 2 |
AIRWAYS |
![]() |
|
P G E 2 |
PLATELETS | Images Inhibits / promotes | |
Inhibits platelet activation in high doses; also shown to promotes platelets | |||
PGF2α |
Directly derived from: Omega-6 AA in meat and eggs. If present, Omega-3 EPA competes for COX-1 or COX-2 enzymes reducing their conversion of Omega-6 AA to PGF2α and other inflammatory /active eicosanoids: PG2, TX2,, LT4. and EX4. | ||
Indirectly derived
from: Omega-6 LA in nuts, seeds,
vegetable oils, or legumes, or Omega-6 DGLA
in breast milk, or GLA
in borage, evening primrose or blackcurrant oil,
which can all ultimately be converted to
Omega-6 AA, and then to
inflammatory /active eicosanoids:
PG2
(incl.
PGF2α), TX2, LT4.
and
EX4 via COX enzymes.. However -
this
omega-6 AA
pathway leading to more inflammatory eicosanoids
competes with
omega-3
presence
for Δ5D, Δ6D
and COX enzymes
that prefer pathways to the more calming,
anti-inflammatory
PG1 (incl.
PGE1), TX1, PG3, TX3 and
LT5 series of eicosanoids. "EFA Conversion Chart" provides a visual aid to understanding these complicated, interacting conversion pathways. |
|||
P G F 2 α |
AIRWAYS
|
![]() |
|
Constricting; Anomaly: Promoted by Cox1 inhibitors (aspirin, traditional NSAIDs) Harrington, 2008 |
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P G F 2 α |
Walls of: BLOOD / LYMPH VESSELS. STOMACH, INTESTINE, BLADDER, UTERUS |
![]() ![]() |
Image contracting SMC |
Via Cox2 -CONSTRICTS Vascular SMCs which
form the supporting tissue of blood vessels in arteries, veins,
lymphatic vessels; uterus CONTRACTS SMCs in other hollow organs: stomach walls, intestine, bladder, uterus |
|||
P G F 2 α |
PLATELETS
|
Image platelet deaggregation | |
INHIBITS platelet activation / blood clotting | |||
P G F 2 α |
EYES | ||
P G F 2 α |
STOMACH Gastric mucosa |
||
Excessive alcohol consumption reduces PGF2α and PGE2 in gastric mucosa; PubMed | |||
PGI2Prostacyclin |
Directly derived from: Omega-6 AA in meat and eggs. If present, Omega-3 EPA competes for COX-1 or COX-2 enzymes reducing their conversion of Omega-6 AA to PGI2 (Prostacyclin) and ALSO reducing conversion to inflammatory /active eicosanoids: PG2, TX2,, LT4. and EX4. | ||
Indirectly derived
from: Omega-6 LA in nuts, seeds,
vegetable oils, or legumes, or Omega-6 DGLA
in breast milk, or GLA
in borage, evening primrose or blackcurrant oil,
which can all ultimately be converted to
Omega-6 AA, and then to mostly
inflammatory /active eicosanoids:
PG2 (includes
calming
PGI2), TX2, LT4.
and
EX4 series via COX enzymes.. However -
this
omega-6 AA
pathway leading to more inflammatory eicosanoids
competes with
omega-3
presence
for Δ5D, Δ6D
and COX enzymes
that prefer pathways to the more calming,
anti-inflammatory
PG1 (incl.
PGE1), TX1, PG3, TX3 and
LT5 series of eicosanoids. "EFA Conversion Chart" provides a visual aid to understanding these complicated, interacting conversion pathways. |
|||
P G I 2 |
BLOOD / LYMPH VESSELS: |
![]() ![]() |
![]() |
PGI2 released by endothelial cells(ECs) lining blood and lymphatic vessels; (Via Cox-1 and Cox-2). Potent inhibitor of platelet aggregation (clot formation), also inhibits fibroblast proliferation, and leukocyte adhesion. | |||
P G I 2 |
SMOOTH MUSCLE CELLS
(SMCs) |
![]() |
|
PGI2 regulates smooth muscle cells; counteracts Thromboxane A2 (TXA2) | |||
P G I 2 |
BRONCHIAL AIRWAYS |
![]() |
|
Released by epithelial cells (EPCs) lining airways, Prostacyclin (PGI2) has a beneficial effect on allergic airway responses and pulmonary hypertension. e.g. in asthma. Zhou, 2016 | |||
P G I 2 |
PLATELETS |
image for deaggregation | |
PGI2 is a POTENT platelet activation inhibitor- reduces platelet aggregation (blood clotting) Via Cox2 | |||
P G I 2 |
KIDNEY, LIVER,
LUNG, HEART |
![]() |
|
P G I 2 |
STOMACH Gastric mucosa |
Image:Gastric mucosa cell protective |
|
Protects stomach and intestinal lining | |||
TXA2Thromboxane(TXA2 ==>TXB2) |
Directly derived from: Omega-6 AA in meat and eggs. If present, Omega-3 EPA competes for COX-1 or COX-2 enzymes reducing their conversion of Omega-6 AA to PGF2α and other inflammatory /active eicosanoids: PG2, TX2,, LT4. and EX4. | ||
Indirectly derived
from: Omega-6 LA in nuts, seeds,
vegetable oils, or legumes, or Omega-6 DGLA
in breast milk, or GLA
in borage, evening primrose or blackcurrant oil,
which can all ultimately be converted to
Omega-6 AA, and then to
inflammatory /active eicosanoids:
PG2, TX2 (incl.
TXA2),, LT4.
and
EX4 via COX enzymes. However -
this
omega-6 AA
pathway leading to more inflammatory eicosanoids
competes with
omega-3
presence
for Δ5D, Δ6D
and COX enzymes
that prefer pathways to the more calming,
anti-inflammatory
PG1 (incl.
PGE1), TX1, PG3, TX3 and
LT5 series of eicosanoids. "EFA Conversion Chart" provides a visual aid to understanding these complicated, interacting conversion pathways. |
|||
T X A 2 |
BLOOD / LYMPH VESSELS |
![]() ![]() ECs via Cox2 |
|
T X A 2 |
PLATELETS | Image: Blood clotting | |
POTENT thrombotic effect in activated platelets via Cox1; involved in thrombosis | |||
T X A 2 |
VSMC proliferation |
TXA2 promotes angiogenesis (creating new blood vessels). This aids damage repair., but is also implicated in tumor formation. Nie et al, 2000 | |
T X A 2 |
AIRWAYS |
![]() |
|
An anomaly is that bronchoconstriction is promoted by Cox-1 inhibitors (aspirin, traditional NSAIDs), but not selective Cox-2 inhibitors. Harrington, 2008. Inhibiting Cox-1 activity seems to promote the LOX pathway over the COX pathway, leading to decreased production of airway anti-inflammatory PGE2 and increased LT production, explaining the observed airway inflammation response | |||
T X A 2 |
PLACENTA | ||
T X A 2 |
KIDNEY | ||
T X A 2 |
Macrophages | ||
Series 3PGs |
Derived from:
Omega-3 EPA e.g. in salmon, fish or krill oil,
Brown / red algae. Grass-fed animals and poultry, land animals'
brains testes, adrenals, eyeballs. Mm Mmm Mmmmm! Compete for COX enzymes in prostanoid (prostaglandin and thromboxane) PG1, TX1, PG2/PG2, TX2 pathways to eicosanoids, |
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PGD3 PGE3 PGF3α PGI3 |
![]() ![]() |
||
MOST CELLS
|
![]() via Cox1 and Cox 2 COUNTER PG-2s / LT-4s. Compete for COX and 5-LOX enzymes. |
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P G E 3 |
PLATELETS | Image deaggregation | |
PGE3 shown to inhibit platelet aggregation. | |||
Leukotrienes | |||
Series 4LTs |
Directly derived from: Omega-6 AA in meat and eggs. If present, Omega-3 EPA competes for 5-LO enzymes reducing their conversion of Omega-6 AA to inflammatory /active LT4 and also EX4 series eicosanoids. | ||
Indirectly derived
from: Omega-6 LA in nuts, seeds,
vegetable oils, or legumes, or Omega-6 DGLA
in breast milk, or GLA
in borage, evening primrose or blackcurrant oil,
which can all ultimately be converted to
Omega-6 AA, and then to
inflammatory /active eicosanoids:
series
PG2 and TX2,
via COX enzymes,
or LT4 and
EX4
via 5-LOX
enzymes. However - this
omega-6 AA
pathway leading to more inflammatory eicosanoids
competes with
omega-3
presence
for Δ5D, Δ6D
and COX and 5-LOX enzymes
that prefer pathways to the more calming,
anti-inflammatory
PG1 (incl.
PGE1), TX1, PG3, TX3 and
LT5 series of eicosanoids. "EFA Conversion Chart" provides a visual aid to understanding these complicated, interacting conversion pathways. |
|||
AIRWAYS | ![]() |
||
Mast cells via 5-LOX (concurrent release
with histamine). Part of the inflammation response, especially in asthma and allergic
rhinitis. Attract white blood cells to sites of tissue damage and
cause smooth muscles to contract. LTC4 and LTD4 increase respiratory mucous secretion. PubMed |
|||
Series 5LTs |
Directly derived from:
Omega-3 EPA e.g. in salmon, fish or krill oil,
Brown / red algae. Grass-fed animals and poultry, land animals'
brains testes, adrenals, eyeballs. Mm Mmm Mmmmm! Compete for 5-LOX enzymes in LT4, EX4 pathways to eicosanoids, |
||
Mast cells via 5-LOX![]() Counters inflammation |
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Specialized Pro-resolving Mediators (SPMs) Deal with reducing excessive tissue injury and resolving inflammation. | |||
Lipoxins |
Derived from: Omega-6 AA in meat and eggs | ||
With sufficient presence of omega-3 EPA : Indirectly derived from: Omega-6 LA in nuts, seeds, vegetable oils, or legumes or Omega-6 DGLA in breast milk or GLA in borage /evening primrose oil. Low dose aspirin can also trigger LIPOXIN synthesis | |||
Neutrophils | Via 15-LOX From AA | ||
Erythrocytes, Reticulocytes | Via 12-LOX From AA | ||
Platelets | Via 12-LOX From LTA5 | ||
Resolvins(RVs) |
Derived from:< Omega-3 EPA or DHA e.g. in salmon, fish or krill oil | ||
Newly discovered. Resolve inflammation, Clear away inflammation debris. Modulates immune system (IS). Serhan et al, 2000 Block prostanoid effects | |||
Protectins(PDs) |
Derived from:< Omega-3 EPA or DHA e.g. in salmon, fish or krill oil | ||
Tissue protective | Protectin D1 (derived from DHA) protects tissue including neuronal tissue from excessive damage Serhan et al. 2002 | ||
Eoxins(EXs) |
Derived from: Omega-6 AA in meat and eggs (competing for | ||
With sufficient presence of omega-3 EPA: Indirectly derived from: Omega-6 LA in nuts, seeds, vegetable oils, or legumes or Omega-6 DGLA in breast milk or GLA in borage /evening primrose oil. | |||
Eosinophils (WBCs), Mast cells | Via 15-LOX-1 Involved in asthma, lymphoma of Hodgkins disease, prostate cancer, colon cancer, and other cancers |
References
Garza, Luis A.; et al. (2012, Mar 12). "Prostaglandin D Inhibits Hair Growth and Is Elevated in Bald Scalp of Men with Androgenetic Alopecia". Science Translational Medicine. 4 (126): 126ra34. PubMed
Green, P., Gispan-Herman, I., & Yadid, G. (2005). Increased arachidonic acid concentration in the brain of Flinders Sensitive Line rats, an animal model of depression. Journal of lipid research, 46(6), 1093-1096. PubMed
Braune S, Küpper JH, Jung F. Effect of Prostanoids on Human Platelet Function: An Overview. Int J Mol Sci. 2020 Nov 27;21(23):9020. doi: 10.3390/ijms21239020. PMID: 33260972; PMCID: PMC7730041. PubMed
Nie D, Lamberti M, Zacharek A, Li L, Szekeres K, Tang K, Chen Y, Honn KV. Thromboxane A(2) regulation of endothelial cell migration, angiogenesis, and tumor metastasis. Biochem Biophys Res Commun. 2000 Jan 7;267(1):245-51. doi: 10.1006/bbrc.1999.1840. PMID: 10623605. PubMed
Chronic low-level inflammation (CLII) involved in almost all health problems
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