Electric cars are poison Thioacetamide Kills Cover up

Metabolism and toxicity of thioacetamide and thioacetamide S-oxide in rat hepatocytes.

Thioacetimide is used for generating G medicinal nanoparticles and in lithium mining. Patent holders are all the usual suspects. Albemarle, Innospec, Dow,DuPont… Etc

The shit is dangerous but they forced it through inspection to make it legal.

Every Kansan should shudder to think what the NBAF will bring to Kansas in its 50-year lifespan. It’s not the threat of an F-5 tornado, or bioterrorist attack that makes the NBAF dangerous to KS agriculture. It’s the knowledge of the scientists conducting “dual use research” there from 2018-2068. http://oba.od.nih.gov/biosecurity/abo… Kansans are to feel safer knowing KSU Alum, former USAMRIID Commander & VP of Midwest Research Institute Global, Col. David R. Franz, is a voting member of the National Science Advisory Board for Biosecurity? The NSABB is charged with “oversight of dual use research, defined as biological research with legitimate scientific purpose that may be misused to pose a biologic threat to public health and/or national security.” http://osp.od.nih.gov/office-biotechn… Col. Franz was a member of the Kansas Bioscience Authority Executive Committee, the group which awarded ~ $450K for 3 studies with his company, Midwest Research Institute, KC, MO. “On April 8, 2009, KBA contracted with MRI for “Task Order No. 2” for a total of $200,000 for “NBAF GOCO Strategy.” ” http://www.kansasbioauthority.org/wp-… How is Midwest Research Institute going to find 300 trustworthy NBAF employees to transfer to KS from its other GOCO labs? Maybe the Kansas Bioscience Authority will pay for security clearances? In 2008, Ventria Bioscience Inc. brought Weiqiang Zhang, seed breeder, to Junction City. Zhang just happened to steal $Million rice seeds, according to the FBI. http://www.therepublic.com/view/story… The KS Bioscience Authority committed $1,000,000 to Ventria. (Approved Oct. 12, 2006.) http://www.kansasbioauthority.org/cit… 2 years, 7 months ago


The hepatotoxicity of thioacetamide (TA) has been known since 1948. In rats, single doses cause centrolobular necrosis accompanied by increases in plasma transaminases and bilirubin. To elicit these effects, TA requires oxidative bioactivation, leading first to its S-oxide (TASO) and then to its chemically reactive S,S-dioxide (TASO(2)), which ultimately modifies amine-lipids and proteins. To generate a suite of liver proteins adducted by TA metabolites for proteomic analysis and to reduce the need for both animals and labeled compounds, we treated isolated hepatocytes directly with TA. Surprisingly, TA was not toxic at concentrations up to 50 mM for 40 h. On the other hand, TASO was highly toxic to isolated hepatocytes as indicated by LDH release, cellular morphology, and vital staining with Hoechst 33342/propidium iodide. TASO toxicity was partially blocked by the CYP2E1 inhibitors diallyl sulfide and 4-methylpyrazole and was strongly inhibited by TA. Significantly, we found that hepatocytes produce TA from TASO relatively efficiently by back-reduction. The covalent binding of [(14)C]-TASO is inhibited by unlabeled TA, which acts as a “cold-trap” for [(14)C]-TA and prevents its reoxidation to [(14)C]-TASO. This in turn increases the net consumption of [(14)C]-TASO despite the fact that its oxidation to TASO(2) is inhibited. The potent inhibition of TASO oxidation by TA, coupled with the back-reduction of TASO and its futile redox cycling with TA, may help explain phenomena previously interpreted as “saturation toxicokinetics” in the in vivo metabolism and toxicity of TA and TASO. The improved understanding of the metabolism and covalent binding of TA and TASO facilitates the use of hepatocytes to prepare protein adducts for target protein identification.




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