Vanadyl Sulfate... Why is this toxic garbage in our supplements?
I recently participated in a thread dealing with this, and I'm glad that the subject of vanadyl sulfate in our supplements, was brought to my attention however.... I wanted to compile all of my information, and present it in a seperate thread (as I feel that it is more appropriately titled, and I am more than willing to confront any company reps on this issue).
It turns out that the majority of companies that are including this substance in their formulations, are doing so, [B]WITHOUT ANY REGUARDS TO TOXICITY.[/B]
Taking .5 to 1 mg a day of vanadyl sulfate is enough to meet or exceed nutritional requirements, without risking toxicity. [B]Most of the bodybuilding supplements contain a [U]minimum[/U] of 5 mg.... [U]and up to 30 mg!!!![/U][/B]
[QUOTE][B]"High doses of vanadium (anything over 15 mg/day) may cause liver and/or kidney damage."[/B]
[color=blue][B]Adult[/B][/color]
Taking 0.5 to 1.0 mg/day of vanadium is enough to meet or exceed nutritional requirements, without risking toxicity. [B]No more than 1.8 mg/day should be used in people. Some manufacturers promote high dosages (15 to 100 mg) of vanadyl sulfate per day, but studies do not support such dosages, and they may be toxic.[/B] Because the safety and effectiveness of vanadium have not been thoroughly studied, caution should be exercised when using vanadium as a nutritional supplement.
[color=blue][B] Uses [/B][/color]
The effects of vanadium have not been studied extensively in people. The majority of studies to date have been conducted in laboratory animals.
[color=blue][B]Body Building/Performance Enhancement[/B][/color]
While vanadyl sulfate is widely used by athletes to enhance performance, beneficial effects have not been confirmed by studies. Use of vanadium is not advised because of the potential toxic effects associated with high doses of this mineral.
[url]http://www.umm.edu/altmed/articles/vanadium-000330.htm[/url][/QUOTE]
[size=+2][B]Material Safety Data Sheet[/B][/size]
[color=blue][B]MSDS Name:[/B][/color] [B][U]Vanadyl Sulfate[/U][/B]
[color=blue][B]Synonyms:[/B][/color] [B][U]Vanadium[/U][/B], Oxo[sulfato(2-)-O]-; Vanadium, Oxosulfato-; Vanadium Oxide Sulfate; Vanadium Oxylsulfate; Oxo(sulfato)
[B]EMERGENCY OVERVIEW[/B]
[size=+2][B]Warning![/B][/size] Causes eye and skin irritation. Causes digestive and respiratory tract irritation. May cause liver and kidney damage.
Target Organs: Kidneys, liver, respiratory system, eyes, skin.
[color=blue][B]Ingestion:[/B][/color] [B]May cause severe gastrointestinal tract irritation with nausea, vomiting and possible burns. May cause liver and kidney damage. May cause central nervous system effects and/or neurological effects. May cause greenish-black tongue discoloration due to deposition of vanadium salts. Ingestion of large amounts may cause an increase in blood pressure.[/B]
[color=blue][B]Eye:[/B][/color] May cause eye irritation and possible damage.
[color=blue][B]Skin:[/B][/color] Contact with skin causes irritation and possible burns, especially if the skin is wet or moist. Contact with the skin may cause skin lesions which are characterized by cracking of the skin and the development of slow-healing ulcers.
[url]https://fscimage.fishersci.com/msds/24800.htm[/url]
[QUOTE=NO HYPE;99277091]I really find it interesting that there are about six NO products on bb.com that contain vanadyl sulfate.... too bad it has been shown to induce pulmonary vaso[U]constriction[/U], as a result of NO [U]inhibition[/U].
Environ Health Perspect. 2004 Feb;112(2):201-6.
[color=blue][B]Vanadyl sulfate inhibits NO production via threonine phosphorylation of eNOS.[/B][/color]
[B]Exposure to excessive vanadium occurs in some occupations and with consumption of some dietary regimens for [U]weight reduction and body building[/U]. Because vanadium is vasoactive, individuals exposed to excessive vanadium may develop adverse vascular effects. We have previously shown that vanadyl sulfate causes acute pulmonary vasoconstriction, which could be attributed in part to inhibition of nitric oxide production.[/B] In the present study we investigated whether NO inhibition was related to phosphorylation of endothelial nitric oxide synthase (eNOS). VOSO4 produced dose-dependent constriction of pulmonary arteries in isolated perfused lungs and pulmonary arterial rings and a right shift of the acetylcholine-dependent vasorelaxation curve. VOSO4 inhibited constitutive as well as A23187-stimulated NO production. Constitutive NO inhibition was accompanied by increased Thr495 (threonine at codon 495) phosphorylation of eNOS, which would inhibit eNOS activity. Thr495 phosphorylation of eNOS and inhibition of NO were partially reversed by pretreatment with calphostin C, a protein kinase C (PKC) inhibitor. There were no changes in Ser1177 (serine at codon 1177) or tyrosine phosphorylation of eNOS. [B]These results indicate that VOSO4 induced acute pulmonary vasoconstriction that was mediated in part by the inhibition of endothelial NO production[/B] via PKC-dependent phosphorylation of Thr495 of eNOS. [B][U]Exposure to excessive vanadium may contribute to pulmonary vascular diseases[/U].[/B][/QUOTE]
Here is more incriminating evidence....
J Inorg Biochem. 1994 Aug 1;55(2):101-12. Links
[color=blue][B]One-electron reduction of vanadate by ascorbate and related free radical generation [U]at physiological pH[/U].[/B][/color]
The one-electron reduction of vanadate (vanadium(V)) by ascorbate and related free radical generation at physiological pH was investigated by ESR and ESR spin trapping. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Incubation of vanadium(V) with ascorbate generated significant amounts of vanadium(IV) in phosphate buffer (pH 7.4) but not in sodium cacodylate buffer (pH 7.4) nor in water. The vanadium(IV) yield increased with increasing ascorbate concentration, reaching a maximum at a vanadium(V): ascorbate ratio of 2:1. Addition of formate to the incubation mixture containing vanadium(V), ascorbate, and phosphate generated carboxylate radical (.COO-), indicating the formation of reactive species in the vanadium(V) reduction mechanism. In the presence of H2O2 a mixture of vanadium(V), ascorbate, and phosphate buffer generated hydroxyl radical (.OH) via a Fenton-like reaction (vanadium(IV)+H2O2-->vanadium(V)+.OH+OH-). The .OH yield was favored at relatively low ascorbate concentrations. Omission of phosphate sharply reduced the .OH yield. [B]The vanadium(IV) generated by ascorbate reduction of vanadium(V) in the presence of phosphate was also capable of generating lipid hydroperoxide-derived free radicals[/B] from cumene hydroperoxide, a model lipid hydroperoxide. Because of the ubiquitous presence of ascorbate in cellular system at relatively high concentrations, one-electron reduction of vanadium(V) by ascorbate together with phosphate may represent an important vanadium(V) reduction pathway in vivo. [B]The resulting reactive species generated by vanadium(IV) from H2O2 and lipid hydroperoxide via a Fenton-like reaction may play a significant role in the mechanism of vanadium(V)-induced cellular injury.[/B]
[B]Oxy-vanadium (IV) complexes having spermicidal activity[/B]
[url]http://www.patentstorm.us/patents/6245808-fulltext.html[/url]
[B]Vanadium promotes hydroxyl radical formation by activated human neutrophils[/B]
[url]http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T38-4HC6J3R-1&_user=10&_coverDate=01%2F01%2F2006&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=07286ce21f8a59f073c9654615a39359[/url]
[B]Vanadium Distribution in Rats and DNA Cleavage by Vanadyl Complex: Implication for Vanadium Toxicity and Biological Effects[/B] [url]http://links.jstor.org/sici?sici=0091-6765(199409)102%3C35%3AVDIRAD%3E2.0.CO%3B2-H[/url]
[B]Vanadium(IV)-mediated free radical generation and related 2'-deoxyguanosine hydroxylation and DNA damage[/B] [url]http://www.ingentaconnect.com/content/els/0300483x/1996/00000106/00000001/art03151[/url]
[B]Vanadium(IV) causes 2'-deoxyguanosine hydroxylation and deoxyribonucleic acid damage via free radical reactions[/B] [url]http://www.annclinlabsci.org/cgi/content/abstract/26/1/39[/url]
Protects against brain damage
Mol Cell Biochem. 2006 Jun;286(1-2):153-9. Epub 2006 Mar 11. Links
Vanadyl sulfate administration protects the streptozotocin-induced oxidative damage to brain tissue in rats.Yanardag R, Tunali S.
Faculty of Engineering, Department of Chemistry, Istanbul University, 34320 Avcilar, Istanbul, Turkey. [email]yanardag@istanbul.edu.tr[/email]
Diabetes mellitus manifests itself in a wide variety of complications and the symptoms of the disease are multifactorial. The present study was carried out to investigate the effects of vanadyl sulfate on biochemical parameters, enzyme activities and brain lipid peroxidation, glutathione and nonenzymatic glycosylation of normal- and streptozotocin-diabetic rats. Streptozotocin (STZ) was administered as a single dose (65 mg/kg) to induce diabetes. A dose of 100 mg/kg vanadyl sulfate was orally administered daily to STZ-diabetic and normal rats, separately until the end of the experiment, at day 60. In STZ-diabetic group, blood glucose, serum sialic and uric acid levels, serum catalase (CAT) and lactate dehydrogenase (LDH) activities, brain lipid peroxidation (LPO) and nonenzymatic glycosylation (NEG) increased, while brain glutathione (GSH) level and body weight decreased. In the diabetic group given vanadyl sulfate, blood glucose, serum sialic and uric acid levels, serum CAT and LDH activities and brain LPO and NEG levels decreased, but brain GSH and body weight increased.The present study showed that vanadyl sulfate exerted antioxidant effects and consequently may prevent brain damage caused by streptozotocin-induced diabetes.