Leukotrienes, white blood cell activity on inflammation
- leuko-: , leuk- ( lū'kō, lūk ), Greek. leukos, white, white blood cells.
- trienes: , triene, Chemistry: 3 double bonds
Inflammation is most often caused by a triene
Whte blood cells attempt to get rid of the triene to combat inflammation
What are trienes?
- a fatty acid
- polyunsaturated: more than one double bond in the carbon chain
- polyene, more than two double bonds in the fatty acid
- mono-ene, one (mono-unsaturated)
- di-ene, two
- tri-ene, three
- quad-ene, four
- poly-ene, many (poly-unsaturated)
- Omega-6: the last double bond is six carbons from the end (caboose) carbon
- plant oils
- Omega-3, the last double bond is three carbons from the end
- animal oils
The two most notorious oils in inflammatory disease are variations of the triene
The key is the fact that they are omega-6 fatty acids (plant seed oil)
- arachidonic acid,
- 4 double bonds
- derived from Linoleic acid,
- 2 couble bonds
- The word "linoleic" derives from the Latin linum "flax" + oleum "oil", first isolated from linseed oil.
- flax seed, linseed, fiber in linnen material, linseed oil is a wood preservative (flax seed oil)
- omega-6 plant oils
- pro-inflammitory response
- astham attack
- diabetic crisis
- cancer tumor formation
Where do we get trienes from?
- discarded waste from lipid bilayer, our membranes
- trienenes block normal oxygen, water, nutrient flow across membranes
- trienenes clog up our membranes to choke off nutrients
- then we swell up, have pain, cannot breathe
- carbon dioxide builds up, cells begin to panic
- consumed in vegetable oils,
- plant oils do not allow membrane transport
- omega-6 seed and nut oils
Symptoms of trienes
- pain, itch, irritation, ache
- redness, heat, hot, burning
- swelling, puffyness, edema
- memory loss, confusion
- weight gain
- elevated triglycerides
A YouTube presentation on the pathway of peanut oil (arachidonic acid)
A PubMed abstract on loss of learning and loss of memory from trienes.
By inhibiting the formation of trienese learning and memory was preserved.
Similar would be to eliminate omega-6 vegetable seed oils from the diet
. 2019 Feb;56(2):1211-1220.
doi: 10.1007/s12035-018-1124-7. Epub 2018 Jun 7.
Learning Impairments, Memory Deficits, and Neuropathology in Aged Tau Transgenic Mice Are Dependent on Leukotrienes
Biosynthesis: Role of the cdk5 Kinase Pathway
Phillip F Giannopoulos 1 , Jian Chiu 1 , Domenico Praticò 2
PMID: 29881943 DOI: 10.1007/s12035-018-1124-7
Previous studies showed that the leukotrienes pathway is increased in human tauopathy and that its manipulation may modulate the onset and development of the pathological phenotype of tau transgenic mice. However, whether interfering with leukotrienes biosynthesis is beneficial after the behavioral deficits and the neuropathology have fully developed in these mice is not known. To test this hypothesis, aged tau transgenic mice were randomized to receive zileuton, a specific leukotriene biosynthesis inhibitor, or vehicle starting at 12 months of age for 16 weeks and then assessed in their functional and pathological phenotype. Compared with baseline, we observed that untreated tau mice had a worsening of their memory and spatial learning. By contrast, tau mice treated with zileuton had a reversal of these deficits and behaved in an undistinguishable manner from wild-type mice. Leukotriene-inhibited tau mice had an amelioration of synaptic integrity, lower levels of neuroinflammation, and a significant reduction in tau phosphorylation and pathology, which was secondary to an involvement of the cdk5 kinase pathway. Taken together, our findings represent the first demonstration that the leukotriene biosynthesis is functionally involved at the later stages of the tau pathological phenotype and represents an ideal target with viable therapeutic potential for treating human tauopathies.
Keywords: Behavior; Five-lipoxygenase; Leukotrienes; Neuroinflammation; Tauopathy; cdk5 kinase pathway.