TreasureVibe
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[1] Bingham, S. "Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response." The Journal of nutrition (2002)
The main suspect behind red meat-induced colon carcinogenesis is the N-nitroso functional group (R–N–N=O), which can be formed on any biomolecule having a terminal amide or imine—i.e. urea, arginine, lysine—and appears to arise from nitrite or nitrogen dioxide. This study had shown very significant increases in N-nitroso compounds after red meat consumption that hadn't been observed after pork- or chicken-eating (but they hadn't checked for prostaglandin E₂).[2] Cross, A. "Haem, not protein or inorganic iron, is responsible for endogenous intestinal N-nitrosation arising from red meat." Cancer Research (2003)
'Although red meat resulted in the expected increase in endogenous N-nitrosation in this study, the same amount of white meat had no effect in 10 of 12 volunteers;' ―Bindham
The same Cambridge researchers followed-up with a very simply yet powerful study design aiming to elucidate some finer details. They had fed white meat, red meat, eggs, lentils, etc., to a group oflimeysEnglish men who'd served as their own controls. Consistent with both epidemiological observation and the N-nitroso hypothesis of colon carcinogenesis, they had found that only those who'd consumed red meat had increased levels of N-nitrosation. This had been a consistent, dose-dependent effect not observed among those eating an isoproteomic amount of anything else.
'Nitric oxide has also been shown to react directly with hemoglobin and myoglobin to produce N-nitroso compounds.' ―Cross
They had also done trials using either simple inorganic iron or that complexed inside a porphyrin ring, or what is called 'haem' by the English. They had found that inorganic iron had done little towards N-nitrosation, but heme–iron had a considerable effect. From this study any logical person is forced to conclude that the heme–iron complex is unique in its ability to catalyze N-nitroso formation.
The total nitrogen consumed has little effect, so it really could be the heme–Fe³⁺ binding to endogenous nitric oxide normally produced from eNOS...
What type of iron do tumors accumulate?
[Cardiotoxicity of lindane, a gamma isomer of hexachlorocyclohexane].
It seems to affect calcium homeostasis of many tissues. The similarity between lindane and inositol (1, 4, 5) phosphate (IP3) suggested that lindane releases Ca2+ from IP3-sensitive intracellular stores in macrophages and myometrial cells. Ca2+ release from reticulum endoplasmic, mitochondria and other Ca2+ stores has been reported in cat kidney cells. Lindane altered energetic metabolism of hepatic mitochondria and the inositol-phosphate synthesis in neuronal cells. However, lindane does not compete with the IP3 receptor. Lindane produces a Ca2+ influx in mice peritoneal macrophage cells responsible for the Ca2+ induced Ca2+ release produced by phospholipase C via IP3 pathway and resulting in a maintained increase of the free cytosolic Ca2+ concentration. Lindane decreased the membrane erythrocyte and cerebral cell concentration of phosphatidyl inositol PI, PIP and PIP2 in rats repetitively exposed to lindane for 3 or 6 months. Lindane induces oxidative stress; it modifies the activity of the scavenger enzymes. This effect is involved in the inhibition of intercellular gap junctions. Modifications of the electrocardiogram (ECG), sinusal rhythm alteration and negative and dysphasic variations of T wave, similar to those produced by hyperkaliemia, have been reported after lindane absorption. During acute lindane poisoning, the activities of serum transaminases (SGOT, SGTP), and lactate deshydrogenase (LDH) increase. Lindane produces histological alterations of cardiac tissues and a cardio-vascular dystrophy (contracture, degenerescence and necrosis) mainly in the left ventricular wall and a hypertrophy of the left ventricle.
source: [Cardiotoxicity of lindane, a gamma isomer of hexachlorocyclohexane]. - PubMed - NCBI
What do you think, does the same go for IP3? I am actually thinking of contacting Dr. Vucenik and Dr. Shamsuddin about this.
Also see:
The cardiac IP3 receptor: Uncovering the role of “the other” calcium release channel
And this: Phytate reduces age-related cardiovascular calcification. - PubMed - NCBI
and Protection of ischemic heart from reperfusion injury by myo-inositol hexaphosphate, a natural antioxidant. - PubMed - NCBI
And Epiphany: Modulation of IP3 receptors in Autism – Pancreatitis and Caffeine?
And: Original article: Caffeine protects against experimental acute pancreatitis by inhibition of inositol 1,4,5-trisphosphate receptor-mediated Ca2+ release
And:
(Oxytocin is a potent uterine stimulator whose clinical use in labor and delivery is well documented. Researchers have shown that oxytocin's clinical effectiveness is due to the activation of phospholipase C to produce inositol-1,4,5-triphosphate which releases calcium from intracellular stores and stimulates uterine contractions. The activation of the phosphatidylinositol signaling system by calcium agonists is also supported by the work of other researchers).
Source: Inositol, IP3 and IP6
This also is kind of confusing, genistein and quercetin lower IP3 in tumors, causing differentiation apoptosis. I thought IP3 was good? Or is this book not correct:
Principles of Orthomolecularism
Also very specific and informative:
Intracellular Signaling Mediators in the Circulatory and Ventilatory Systems
And this is also significant:
Huntington's disease[edit]
Huntington's disease occurs when the cytosolic protein Huntingtin (Htt) has an additional 35 glutamine residues added to its amino terminal region. This modified form of Htt is called Httexp. Httexp makes Type 1 IP3receptors more sensitive to IP3, which leads to the release of too much Ca2+ from the ER. The release of Ca2+ from the ER causes an increase in the cytosolic and mitochondrial concentrations of Ca2+. This increase in Ca2+ is thought to be the cause of GABAergic MSN degradation.[15]
Source: Inositol trisphosphate - Wikipedia
Heart disease is a major complication in Huntington's Disease according to Huntington's disease - Wikipedia
The second greatest risk is heart disease, which causes almost a quarter of fatalities of those with HD.[17]
Another good source on the specific matter:
Intracellular Calcium
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