VacTruth Notice
We are publishing this information to educate Congress, the media, and public regarding issues affecting the health and well-being of our citizens. It is not our intention to infringe upon anyone’s copyright. We believe we have used the U.S. Copyright’s Doctrine of Fair Use equitably and without incurring infringement or plagiarism. All sources are cited in detail.
VacTruth Comment:
Tween 80, Triton X-100, and Nonoxynol-9 are used in vaccines. Nonoxynol-9 (N-9) also is used as a spermicide in vaginal gels to prevent contraception and was used in a H1N1 Vaccine Trial.
Triton X-100 and Tween 80 were mixed with DDT to spray on crops in the 1940s and 1950s – combinations of these chemicals are still in pesticides today. Polysorbate 80, also known as Tween 80, is a surfactant in these vaccines: DTaP, DTaP-HebB-IIPV, DTaP-Hib, Gardasil, Influenza, Rotavirus, and Tdap.
Most of the following information regarding these non-ionic surfactants is taken from the National Institutes of Health web sites.
Specific role of polysorbate 80 coating on the targeting of nanoparticles to the brain
http://www.ncbi.nlm.nih.gov/pubmed/14967540
“Being bound to nanoparticles that were overcoated by T-80 [Tween-80] later, was necessary for the loading to be delivered to brain. Partial coverage was enough for T-80 coating to play a specific role in brain targeting. It seemed that brain targeting of nanoparticles was related to the interaction between the T-80 coating and BMECs [brain micro-vessel endothelial cells]. The mechanism of endocytosis was more reasonable for nanoparticle-mediated drugs across BBB [Blood Brain Barrier]. The specific role of T-80 coating on nanoparticles in brain targeting was thus confirmed.” [Emphasis added]
Colloidal carriers and blood–brain barrier (BBB) translocation: A way to deliver drugs to the brain?
http://www.ncbi.nlm.nih.gov/pubmed/15896933
“3.1.1. Disruption of the BBB
One of the earliest techniques to circumvent the BBB for therapeutical purpose and the first to be used in humans was developed by Neuwelt et al. (1979). The idea behind this approach was to break down the barrier temporarily by injecting a sugar solution (mannitol) into arteries in the neck. The resulting high sugar concentration in brain capillaries sucks water out of the endothelial cells, shrinking them thus opening tight junctions. In current practice, the effect lasts for 20–30 min, during which time drugs that would not normally cross the BBB diffuse freely.”
…
“However, disrupting the BBB even for brief periods leaves the brain vulnerable to infection and damage from toxins. Even substances that circulate harmlessly through the peripheral bloodstream, such as albumin, can have deleterious effects if they enter the brain.” [Emphasis added]
…
VacTruth Comment:
Neurotoxins in vaccines can enter the brain easily, which this confirms.
“The “Trojan horse” mechanism postulates that infected macrophages crossactivate brain endothelial cells to take up residence in the CNS as infected microglial cells. BMEC and immune cells, activated by cytokines, overexpress adhesion molecules and their ligands, which promotes the binding of circulating immune cells to brain vasculature.Such binding could be the first step in diapedesis, the passage of immune cells across the BBB. This proximity could also facilitate the passage of viral particles between the infected immune cell and the brain endothelial cell, analogous to the transfer of virus betweeninfected immune cells.” [Emphasis added]
…
“After peripheral administration, these molecules themselves do not exhibit any therapeutic effect because they do not diffuse through the BBB. But, when dalargin or loperamide were absorbed onto the surface of poly(butylcyanoacrylate) (PBCA) nanoparticles further coated with the detergent, polysorbate-80 (PS-80), a pronounced analgesic effect was obtained, reaching a maximum 45 min after administration. The mechanism behind the translocation of those nanoparticles into the brain remains, however, not fully understood.”
Disclosure by triton X-100 of NMDA-sensitive [3H] glutamate binding sites in brain synaptic membranes.
http://www.ncbi.nlm.nih.gov/pubmed/2838020
“Pretreatment of brain synaptic membrane homogenates with Triton X-100 resulted in a drastic disclosure of [3H]glutamate (Glu) binding activity which was sensitive to one of the central GIu receptor agonists, N-methyl-D-aspartic acid (NMDA)… These results suggest that Triton-treatment may disclose NMDA-Sensitive [3H]GIu binding sites in brain synaptic membranes.”
VacTruth Comment:
Polysorbate 80 and Tween 80 are regarded as the same chemical. For vaccines, see information under Polysorbate 80.
Interference of the Detergent Tween 80 in Protein Assays
http://www.ncbi.nlm.nih.gov/pubmed/1481978
“Detergents are often used to dissociate cell membrane components in biological systems. The nonionic detergent, polyoxyethylene sorbitan monooleate (Tween 80) has been widely used at concentrations of 0.051.0% to increase secretion of enzymes or other exoproteins in both bacteria and fungi.”
“Tween 80 is one of the polyoxyethylene family of nonionic detergents which includes, among others, the Tritons (X-100 and X-114) and the Genapols (X-080, X-100, and X-150). These detergents are gentle in their action, and most enzymes retain their activity after exposure to levels of l-3% w/v (26). Because of their mild action and their compatibility with most chromatographic systems, these detergents have found widespread application as extractive agents for proteins which are structurally associated with organelles such as mitochondria, chloroplasts, plasmalemma, endoplasmic reticulum, and nuclear membrane.” [Emphasis added]
Tween 80 Immunosuppression
Food and Chemical Toxicology, Vol 20. No. 6 pp. 983.
“Tween 80 (polyoxyethylene sorbitan monooleate), an emulsifier, is yet another example or a commonly used chemical being implicated in the suppression of the immunological response. Barnett reports that recent work in his laboratory has suggested that the primary IgE and IgG, MS suppressed in mice pretreated with Tween 80 followed by an immunizing dose of ovalbumin adsorbed to aluminium hydroxide (an antigenadjuvant combination known to produce high levels of IgE and IgG,)… The authors conclude from these findings that the immunosuppression caused by Tween 80 is restricted to the primary humoral response.” [Emphasis added]
VacTruth Comment:
The adjuvant aluminium hydroxide is in the following vaccines: Anthrax, DTaP, DTaP-HepB-IPV, Td, Hepatitis A, Hepatitis A-Hepatitis B, Hepatitis B, Tdap.
Tween 80 and Epileptic Seizures
Some solvents for antiepileptics have proepileptic potencies in the WAG/Rij rat model for absence epilepsy
http://www.ncbi.nlm.nih.gov/pubmed/1393624
“To suppress these symptoms [of epilepsy], anticonvulsants or antiepileptics have been developed…that can be used in experimental studies as a solvent, emulsifier, or dispersing agent for these difficult to dissolve drugs. Tween-80 is used to dissolve benzodiazepines and P-carbolines. Carbamazepine and trimethadione are dissolved in a mixture of saline, ethanol, and propylene glycol.
…
These solvents, however, are also known to disrupt the bloodbrain barrier, change receptor affinity, and manipulate membrane structure…It is not clear why the used solvents are proepileptic but their usage in experimental absence epilepsy research should be avoided.” [Emphasis added]
Delayed effects of neonatal exposure to Tween 80 on female reproductive organs in rats
http://www.ncbi.nlm.nih.gov/pubmed/8473002
“Tween 80 is a classical non-ionic surface-active detergent. It is widely used as an additive in pharmaceuticals and in the food industry. Some of the Tweens are considered to be carcinogens or cocarcinogens. Several of the stimulating properties of tweens are already known.” [Emphasis added]
and …
“In our study, we found that 4-day administration of Tween 80 to female rats during the period crucial for the development and function of reproductive organs accelerates the maturation of these organs. We found significant prolongation of the oestrous cycle and induction of persistent vaginal oestrus. The persistence of vaginal oestrus after the perinatal exposure of female rats to oestrogens used to be ascribed to oestrogens.” [Emphasis added]
VacTruth Question:
Could Tween 80, being a carcinogen or co-carcinogen, also be one of the reasons vaccines are not tested for causing cancer? Please research the vaccine inserts (http://vactruth.com/vaccine-inserts) to confirm.
Treatment of Cells with Detergent Activates Caspases and Induces Apoptotic Cell Death
http://www.ncbi.nlm.nih.gov/pubmed/10833528
“The biochemical properties of detergents and biomembranes suggest that the initial event of apoptosis induction may occur at the cell membrane. Although the Triton concentration required for apoptosis induction did not immediately disrupt the cell membrane, detergent molecules may be incorporated into the lipid bilayer. This may result in subtle alterations of the physical properties of the membrane including an increased permeability for small charged and neutral solutes… In conclusion, treatment of human and nonhuman cells with detergent at concentrations below the level that causes cytolysis induced apoptotic death.”
Cancer and Tween-80 Injections
Effects of repeated subcutaneous injection of Tween-80 in rats
http://www.ncbi.nlm.nih.gov/pubmed/5914564
“In the rats injected with Tween-80, 1 subcutaneous sarcoma was found at the site of injection, and 2 similar sarcomas were also found in the rats injected with Tween-80 and small amounts of 3′-me-DAB. In mice 2 subcutaneous sarcomas were induced by injections of Tween-80 alone. These results raise the possibility that Tween-80 may be directly involved in carcinogenesis.” [Emphasis added]
Triton X-100 and Tween 80 Damage the Gut (Ciba-Geigy Corporation)
Evaluation of mucosal damage of surfactants in rat jejunum and colon
http://www.ncbi.nlm.nih.gov/pubmed/7766919
“In particular, surfactants, which are commonly used adjuvants in oral pharmaceutical preparations to improve wetting and solubilization for insoluble drugs, have come under investigation as absorption enhancers. The goal of an enhancer is to improve membrane permeability without unwanted side effects. However, this is a formidable task because absorption is often increased due to intestinal damage.”
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“Tween 80 is an orally approved surfactant routinely used in drug formulations and food products (FDA Inactive Ingredient Guide, 1991). In contrast, Triton X-100 is not approved for oral use and is regarded as toxic.”
…
“Denudation of villous tips, desquamation of the epithelial surface, and intervillous adhesion by LM and SEM were noted with Triton X-100 exposure, while minimal changes were noted with Tween 80 and controls. These results are consistent with the known systemic toxicity of Tween 80 and Triton X-100 and suggest that this method is valuable for the early assessment of intestinal damage and irritation.”
VacTruth Comment:
Triton X-100 is a nonionic surfactant used in influenza vaccines.
Encyclopedia of Pharmaceutical Technology Vol. 11
Authors James Swarbrick & James C. Boylan
1995 New York: Marcel Dekker, Inc.
“The addition of surfactants to ophthalmic solutions is permitted, even though their use is greatly restricted. The toxicity of surfactants is on the order anionic > cationic > nonionic. Nonionics are used in low concentrations to increase the dispersion of suspended drugs, such as steroids, and thereby improve solution clarity. The ability of these compounds to bind and thereby inactivate certain preservatives, coupled with their irritation potential, limits their use to low concentrations. For example, the FDA limits the concentrations of Tween 20 and Tween 80 to 1%.” (page 61)
“In the early 1980s, reports appeared in the literature about deaths in neonates associated with the administration of IV E-Ferol, a product that contained Vitamin E (dl-a-tocopherol) and the emulsifiers polysorbate 80 (9%) and polysorbate 20 (1%). Some infants who received this vitamin E product developed coagulopathy, renal failure, hepatic failure, and death. On autopsy, the infants who died from hepatic failure demonstrated cholestasis similar to that associated with parenteral nutrition. Toxic reactions may have occurred because of the high doses of vitamin E, the presence of polysorbate(s), a contaminant in the pharmaceutical preparation, or a combination of all three.” (page 345) [Emphasis added]
VacTruth Comment:
Medical personnel often ignore the potential side effects of the chemicals in vaccines because of the ‘trace’ amounts in vaccines, or because an ingredient is labeled inactive. The same text referenced above notes,
“Pharmaceutical products may contain, in addition to the active or therapeutic agent(s), a variety of other ingredients, termed inactive or inert, which are categorized as excipients or additives (flavorings, sweeteners, preservatives, stabilizers, diluents, lubricants, etc.). The words inert or inactive may be misnomers for some excipients because some have been shown to cause adverse effects. Neonates and young children are at risk for such effects because they may not be able to metabolize or eliminate an ingredient in a pharmaceutical product in the same manner as an adult.” (pp. 344) [Emphasis added]
Nonoxynol-9 Induces Apoptosis of Endometrial Explants by Both Caspase-Dependent and -Independent Apoptotic Pathways
http://www.biolreprod.org/content/73/2/382.full.pdf
“This study demonstrates for the first time that N-9 induces apoptosis in human endometrial explants. As a membrane- active surfactant spermicide, N-9 induces membrane permeability and membrane fusion. It is well known that cell membrane integrity is essential to maintain intracellular homeostasis, viability, and function. It was recently reported that detergents such as Triton X-100, Nonidet P-40 (NP-40), n-octylglucoside, and the bile salt sodium deoxycholate similarly induce apoptosis, indicating that apoptosis induction in the setting of this study may be not a feature peculiar to N-9 but a more general effect of the interaction of detergents with tissue … such damage could facilitate infection with bacterial or viral pathogens such as HIV.” [Emphasis added]
VacTruth Comment:
Apoptosis means cell death or cell ‘suicide’.
and
“The N-9-triggered apoptosis of endometrial explants appears to be mediated through involvement of FAS/FASLG mechanism, followed by CASP3 activation leading to final cell death…These findings may have important practical implications to future microbicide development by demonstrating that vaginally administered agents may cause upper reproductive tract toxicity and possibly facilitate HIV infection.” [Emphasis added]
Solubilization of membranes by detergents
http://www.ncbi.nlm.nih.gov/pubmed/1091302
“Lysis by surfactants has been studied mainly using erythrocytes [Red Blood Cells], since the process can be measured quantitatively by following the release of haemoglobin… The lytic process can, however, be divided into five stages: (1) The surfactant monomers absorb to, and (2) penetrate into the membrane, where (3) they induce a change in molecular organization. This leads to an alteration in permeability (4) and in the osmotic equilibrium, and finally (5) to the leakage of haemoglobin. Stages 2, 3 or 4 are rate limiting. It is generally believed that lysis results from an interaction between surfactant and the lipids of the membrane. Haydon and Taylor have suggested that surfactants may act as ‘wedges’ which destroy the natural orientation of the lipid bilayer.”
VacTruth Comment:
Lysis means dissolution or breakdown of cells.
Vascular endothelial dysfunction contributes to myocardial depression inischemia-reperfusion in the rat
http://www.ncbi.nlm.nih.gov/pubmed/9564547
“This study was designed to evaluate whether the direct contractile modulatory effects of endocardial and (or) vascular endothelium were altered and whether these alterations contributed to contractile dysfunction in a model of ischemia-reperfusion. Sixty-two perfused rat hearts as Langendorff preparations were randomized to no intervention, intracoronary Triton X100 injection (to render vascular endothelium dysfunctional), ischemia (30 min)-reperfusion (20 min), and ischemia-reperfusion followed by intracoronary Triton X100 injection. Coronary endothelial-dependent vascular reactivity and vascular smooth muscle reactivity were assessed by serotonin and sodium nitroprusside, respectively. Myocardial damage was assessed by coronary effluent creatine phosphokinase and by morphologic studies. Papillary muscles were then excised and contractile characteristics evaluated at varying extracellular calcium concentration prior to and after endocardial endothelial removal with Triton X100…We conclude that vascular but not endocardial endothelial dysfunction contributes to the myocardial dysfunction that occurs during ischemia-reperfusion injury.” [Emphasis added]
VacTruth Comment:
Ischemia is tissue damage due to lack of adequate blood flow (which brings oxygen and nutrients to the tissue).
PATHOGENESIS OF HIPPOCAMPAL NEURONAL DEATH AFTER HYPOXIA–ISCHEMIA CHANGES DURING BRAIN DEVELOPMENT
http://www.ncbi.nlm.nih.gov/pubmed/15219674
“Apoptotic neuronal death takes place during brain development under genetic control. Nuclear chromatin condensation or clumping characterized by electron microscopy (EM) is a hallmark of apoptosis and is remarkably conserved among cell types (Kerr et al., 1972; Wyllie, 1997). It is well documented that pathological conditions including brain hypoxia–ischemia (HI) are able to initiate apoptotic machinery to facilitate cell death through activation of caspase-3 (Blomgren et al., 2003; Olney, 2003). In comparison with apoptosis, necrotic cell death occurs always under pathological conditions.Two types of neuronal injury-induced necrotic morphologies characterized by EM have been described in the literature: one is the conventional cellular lysis with cell swelling followed by rupture to release cell contents; the second type of necrosis is characterized by dilation of subcellular organelles followed by shrinkage of the entire cell. Neuronal cell lysis takes place in the infarct core area after focal brain ischemia (Dodson et al., 1974), while the shrinkage type of necrosis occurs in a delayed manner in vulnerable brain regions after transient brain ischemia, in the penumbral regions after focal ischemia, as well as in regions of excitotoxic neuronal death (Siesjo¨, 1985; Deshpande et al., 1992; Fukuda et al., 1999; Colbourne et al., 1999; Hu et al., 2000b; Olney, 2003). In some cases, mixed features of apoptosis and necrosis can be seen in the same neurons after brain injury (Martin et al., 1998;Ishimaru et al., 1999). The neurons dying during development also adopt one of at least three different morphological types: “apoptotic,” “autophagic,” and “non-lysosomal vesiculate,” which probably reflect the various mechanisms underlying both nuclear and cytoplasmic destruction during cell death in developing neurons (Clarke, 1990). [Emphasis added]
….
It is, therefore, likely that immature neurons are liable to apoptosis after injury (Ikonomidou et al., 1989; Johnston, 1995), and thus both necrosis and apoptosis remain effective therapeutic targets for developing neurons after brain injury (Han et al., 2000; Cheng et al., 1998; Nakajima et al., 2000; Northington et al., 2001; Blomgren et al., 2001). However, both apoptotic morphology and biochemical machinery fade out during brain development. Therefore, traditional approaches targeting to necrotic cell death mechanisms such as energy failure, acidosis, calcium influx, oxidative stress and protein aggregation in adult brain remain valid.”
Ischemic preconditioning prevents protein aggregation after transient cerebral ischemia.
http://www.ncbi.nlm.nih.gov/pubmed/15939539
“A short period of ischemia (ischemic preconditioning) that does not lead to neuronal death (sublethal), is able to induce neuronal tolerance to a subsequent longer or lethal period of ischemia. This phenomenon is known as “ischemic tolerance.” Although definitive mechanisms underlying ischemic tolerance remain incompletely understood, induction of molecular chaperones and folding enzymes has long been proposed to contribute to the acquisition of ischemic tolerance.” [Emphasis added]