1. Tetrafluoroethene
2. Tetrafluoroethylene, Ion(1+)
3. Tetrafluoroethylene, Ion(1-)
1. Tetrafluoroethene
2. 116-14-3
3. Perfluoroethylene
4. Perfluoroethene
5. Ethene, Tetrafluoro-
6. 1,1,2,2-tetrafluoroethylene
7. Fluoroplast 4
8. Ethylene, Tetrafluoro-
9. Poly(tetrafluoroethylene)
10. C2f4
11. 9002-84-0
12. 1,1,2,2-tetrafluoroethene
13. Polytetrafluoroethylene
14. Perfluoraethylen
15. Tetrafluoraethen
16. Tetrafluoraethylen
17. F2c=cf2
18. Omw63z518s
19. Chebi:38866
20. Ethene, 1,1,2,2-tetrafluoro-
21. Ethene,1,1,2,2-tetrafluoro-, Oxidized, Polymd.
22. Tetrafluorethene
23. Mfcd00084455
24. Tetrafluoroethylene Monomer
25. Ccris 7738
26. Hsdb 844
27. Einecs 204-126-9
28. Un1081
29. Unii-omw63z518s
30. Polytef
31. Tetrafluorethylene
32. Tetrafluoro Ethene
33. Teflon
34. Ec 204-126-9
35. Ms-122 (salt/mix)
36. Tetrafluoroethyl Methyl Ether
37. Tetrafluoroethylene, Inhibited
38. Un 1081 (salt/mix)
39. Chembl541730
40. Tetrafluoroethylene [mi]
41. Dtxsid6021325
42. Tetrafluoroethylene [hsdb]
43. Tetrafluoroethylene [iarc]
44. 1,1,2,2-tetrakis(fluoranyl)ethene
45. Mfcd00039272
46. Ptfe Rod, 19mm (0.75in) Dia
47. Zinc40454334
48. Polytetrafluoroethylene, 6-10 Micron
49. Tetrafluorethylene Telomer (salt/mix)
50. Akos006227790
51. Ptfe Rod, 12.7mm (0.5in) Dia
52. Ptfe Rod, 25.4mm (1.0in) Dia
53. Ptfe Rod, 6.35mm (0.25in) Dia
54. Ptfe Sheet, 12.7mm (0.5in) Thick
55. Ptfe Rod, 3.18mm (0.125in) Dia
56. Ptfe Sheet, 1.6mm (0.063in) Thick
57. Ptfe Sheet, 6.35mm (0.25in) Thick
58. Ptfe Sheet, 0.81mm (0.031in) Thick
59. Ptfe Sheet, 3.18mm (0.125in) Thick
60. 1,1,2,2-tetrafluoro-1,2-ethanediylradical
61. C19299
62. 116t143
63. A803563
64. Q412460
65. Tetrafluoroethylene, Inhibited [un1081] [flammable Gas]
| Molecular Weight | 100.01 g/mol |
|---|---|
| Molecular Formula | C2F4 |
| XLogP3 | 1.3 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 4 |
| Rotatable Bond Count | 0 |
| Exact Mass | 99.99361265 g/mol |
| Monoisotopic Mass | 99.99361265 g/mol |
| Topological Polar Surface Area | 0 Ų |
| Heavy Atom Count | 6 |
| Formal Charge | 0 |
| Complexity | 55.6 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
EXPL THER Here, we described the in vitro biocompatibility of a novel nanostructured surface composed of PTFE as a potential polymer for the prevention of adverse host reactions to implanted devices. The foreign body response is characterized at the tissue-material interface by several layers of macrophages and large multinucleated cells known as foreign body giant cells (FBGC), and a fibrous capsule. The nanofibers of nanofibrous PTFE (nPTFE) range in size from 20 to 30 nm in width and 3-4 mm in length. Glass surfaces coated with nPTFE (produced by jet-blowing of PTFE 601A) were tested under in vitro conditions to characterize the amount of protein adsorption, cell adhesion, and cell viability. We have shown that nPTFE adsorbs 495 +/- 100 ng of bovine serum albumin (BSA) per sq cm. This level was considerably higher than planar PTFE, most likely due to the increase in hydrophobicity and available surface area, both a result of the nanoarchitecture. Endothelial cells and macrophages were used to determine the degree of cell adsorption on the surface of the nanostructured polymer. Both cell types were significantly more round and occupied less area on nPTFE as compared to tissue culture polystyrene (TCPS). Furthermore, a larger majority of the cells on the nPTFE were dead compared to TCPS, at dead-to-live ratios of 778 +/- 271 to 1 and 23 +/- 5.6 to 1, respectively. Since there was a high amount of cell death (due to either apoptosis or necrosis), and the foreign body response is a form of chronic inflammation, an 18 cytokine Luminex panel was performed on the supernatant from macrophages adherent on nPTFE and TCPS. As a positive control for inflammation, lipopolysaccharide (LPS) was added to macrophages on TCPS to estimate the maximum inflammation response of the macrophages. From the data presented with respect to IL-1, TNF-alpha, IFN-gamma, and IL-5, we concluded that nPTFE is nonimmunogenic and should not yield a huge inflammatory response in vivo, and cell death observed on the surface of nPTFE was likely due to apoptosis resulting from the inability of cells to spread on these surface. On the basis of the production of IL-1, IL-6, IL-4, and GM-CSF, we concluded that FBGC formation on nPTFE may be decreased as compared to materials known to elicit FBGC formation in vivo.
PMID:17209629 Ainslie KM et al; Langmuir. 23 (2): 747-54 (2007)
We previously showed that ringed polytetrafluoroethylene (PTFE) grafts combined with small allograft patches showed high patency rates similar to those of iliac vein grafts and therefore that they can be used for middle hepatic vein (MHV) reconstruction. Although such use of PTFE graft showed high patency rates, its long-term safety regarding infection and other types of complications were not presented. In this study, we investigated the actual risk of complications directly associated with PTFE graft interposition for MHV reconstruction. METHODS: During the study period of 30 months, we performed 215 cases of adult living-donor liver transplantation with modified right lobe graft and PTFE grafts. We classified the potential complications directly associated with PTFE graft interposition as infectious and surgical complications. The medical records of study patients were retrospectively reviewed. RESULTS: MHV graft patency rate was 76.3% at 6 months and 36.7% at 12 months. Their 1-year graft and patient survival rates were 92.6% and 93.5%, respectively. The 1-year actual incidences of infectious complication and surgical complication were near zero and 1 case (0.5%), respectively. In 1 recipient, the PTFE graft penetrated into the stomach wall 6 months after transplantation, but the patient did not complain of any specific symptoms. The PTFE graft was removed with the use of laparotomy, and the patient recovered uneventfully. CONCLUSIONS: Although the incidence of PTFE graft-associated complication rate is very low, we suggest that it is necessary to closely monitor the PTFE graft, because unexpected complications can happen during long-term follow-up.
PMID:24767363 Ha TY ET AL; Transplant Proc. 46 (3): 845-9 (2014)
A 73-year-old female with sick sinus syndrome and atrial fibrillation was implanted with a ventricular demand inhibit pacemaker. She subsequently developed multiple episodes of skin irritation and necrosis. Skin patch testing revealed sensitivity to almost every component of the pacemaker system. The pacemaker was removed and replaced with a new pacemaker in which the generator was covered with a polytetrafluoroethylene (PTFE) sheet and the lead was covered with PTFE conduit. The patient suffered no further episodes of pacemaker-associated contact dermatitis.
PMID:24899091 Taguchi T et al; J Artif Organs. 17 (3): 285-7 (2014)
The teflon hip arthroplasty design was used by Sir John Charnley in the early 60's but was taken off the market due to high complication rates. A case is reported of an intrapelvic granuloma after total hip arthroplasty following the use of a teflon socket. This appears to be the last surviving patient treated by Sir John Charnley using a Teflon hip socket design. /Former use/
PMID:20306978 Gheorghiu D et al; Acta Orthop Belg. 76 (1):129-31 (2010)
Management of unilateral vocal fold paralysis continues to generate controversy. Various techniques, but essentially teflon injection and thyroplasty I have been widely used for medialization. Assessment procedures largely differ from author to author: a few authors report objective superiority of thyroplasty (small series). In our own material (19 teflon injections and 9 thyroplasties), when considering objective functional outcomes and patient satisfaction, we cannot demonstrate a statistically significant superiority of one of the techniques, both of them giving very satisfactory results. When considering the literature, the main problem with teflon is delayed (up to 25 years) occurence of granulomas, which is reported as not unfrequent and to some extent unpredictible. Management of teflon granulomas is difficult. Most major complications of thyroplasty (airway obstruction/prosthesis extrusion) occur quite early after surgery and can better be controlled.
PMID:9865105 Dejonckere PH; Rev Laryngol Otol Rhinol (Bord). 119 (4): 265-9 (1998)
Soft tissue reactions to materials in joint prostheses include discoloration, fibrosis, florid histiocytic reaction, and granulomatous inflammation with foreign body giant cell reaction. Clinical manifestations include pain and swelling. We report a case of temporomandibular joint Proplast-Teflon prosthesis, followed by the development of large cell lymphoma in the left parotid gland 10 years after joint replacement. While it is unclear whether the implant directly contributed to the development of lymphoma, this association has not been previously documented, prompting this report.
PMID:22533111 Ong MG et al; J La State Med Soc. 164 (1): 31-2 (2012)
Expanded polytetrafluoroethylene implant is usually considered as a wonderful implant for chin cosmetic augmentation with no or less bone resorption compared with solid silicone implant. However, one severe bony erosion in expanded polytetrafluoroethylene chin augmentation was found in our clinical work. We consider that the possible reason about severe bone resorption in such situation is most relative to the mentalis muscle hyperactivity, rather than the kinds of materials. We also strongly advise that genioplasty is suitable for the cases with mentalis muscle hyperactivity caused by a dentofacial deformity.
PMID:24036760 Shi L et al; J Craniofac Surg. 24 (5): 1711-2 (2013)
Positron emission tomography with (18)F-fluorodeoxyglucose (18FDG) has been increasingly used in the diagnostic investigation of patients with neoplasms of the head and neck. Positron emission tomography and computed tomography have also proven useful for surveillance of thyroid cancers that no longer concentrate radioiodine. However, certain benign or inflammatory lesions can also accumulate (18)F-fluorodeoxyglucose and lead to misdiagnosis. We review and discuss the pitfalls of using positron emission tomography and computed tomography for surveillance of thyroid cancer. We present the case of a 48-year-old woman who was diagnosed with a laryngeal neoplasm on integrated positron emission tomography and computed tomography scanning, after a routine ultrasound demonstrated an enlarged thyroid nodule. On physical examination, she had a laryngeal mass overlying an immobile vocal fold. The mass was biopsied and found to harbour a Teflon granuloma. Positron emission tomography positive Teflon granulomas have previously been reported in the nasopharynx and vocal folds, and should be considered in the differential diagnosis of patients who have undergone prior surgery involving Teflon injection. It is important for otolaryngologists and radiologists to recognise potential causes of false positive positron emission tomography and computed tomography findings, including Teflon granulomas.
PMID:18976510 Ondik MP et al; J Laryngol Otol. 123 (5): 575-8 (2009)
Exposure to pyrolysis products equiv to 50 ppm carbonyl fluoride for 1 hr daily incr the fluoride ion content of urine of rats from 3 to 42 ug/ml in 5 days...
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V19 295
Fluoride levels in urine are greater than normal in workers exposed to fumes of polytetrafluoroethylene.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V19 296
/Teflon/ paste material can be transported by lymphatics.
Rossoff, I.S. Handbook of Veterinary Drugs. New York: Springer Publishing Company, 1974., p. 467
Male rats exposed to 14 000 mg/cu m tetrafluoroethylene in air for 30 min excreted small amounts of fluoride ion in the urine over a 14-day period, indicating that metabolism can occur.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V71 (99) 1145
Tetrafluoroethylene was metabolized to S-(1,1,2,2-tetrafluoroethyl)glutathione by rat liver fractions in vitro; the reaction was catalyzed by both microsomal and cytosolic glutathione S-transferases. The rate with microsomes was four times that with cytosol fractions. Evidence for this metabolic pathway in vivo has been obtained by the identification of the cysteinylglycine and cysteine conjugates of tetrafluoroethylene in rat bile. Cytochrome P-450 oxidation, a common metabolic route for haloalkenes, does not appear to occur in the metabolism of tetrafluoroethylene ... When administered po to rats, the synthetic cysteine conjugate of tetrafluoroethylene causes renal damage identical to that caused by tetrafluoroethylene itself. The conjugate was metabolized by renal slices in vitro giving pyruvate, ammonia, and a reactive species which caused marked inhibition of organic ion transport into slices. Purified renal beta-lyase also cleaved this conjugate giving stoichiometric amounts of pyruvate and ammonia ... The nephrotoxicity of tetrafluoroethylene is believed to derive from the hepatic glutathione conjugate of this compound. Following excretion and degradation of this conjugate in bile, the cysteine conjugate is reabsorbed and further metabolized in the kidney by the enzyme beta-lyase to a cytotoxic species.
PMID:6495336 Odum J, Green T; Toxicol Appl Pharmacol 76 (2): 306-18 (1984)
The metabolism of tetrafluoroethylene has been studied in rat liver fractions; both microsomal and cytosolic glutathione S-transferases catalyze the formation of S-(1,1,2,2-tetrafluoroethyl)glutathione. The rate with microsomes was four times greater than with cytosol. Fluoride ion release was equivalent to approximately 20% of the glutathione used. The quantities of glutathione used and of fluoride ion released in incubations were identical whether cytochrome P450 was active or had been inactivated with carbon monoxide. Thus, cytochrome P450 oxidation, a pathway common to many haloalkenes, does not appear to be involved in the metabolism of tetrafluoroethylene. Evidence for the glutathione conjugation pathway in vivo comes from the identification of the cysteinylglycine and cysteine conjugates of tetrafluoroethylene in rat bile, following oral administration of L-[35S]cysteine and then inhalation exposure to 6000 ppm [24 600 mg/cu m] tetrafluoroethylene for 6 hr. S-(1,1,2,2-Tetrafluoroethyl)-L-cysteine is metabolized in vitro in rat renal cortex slices to give pyruvate and ammonia, a reaction that is catalyzed by beta-lyase and which also generates a reactive thiol that is probably important in renal cytotoxicity.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V71 (99) 1146
... Tetrafluoroethylcysteine to male rats ... is an important metabolite in the cytotoxic response. The cytotoxicity of the cysteine conjugate has also been demonstrated in vitro in rat kidney slices by reduced uptake of both organic anion, para-aminohippuric acid and the cation, tetraethylammonium bromide.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V71 (99) 1147-1148
The major gaseous degradation products of PTFE are hydrogen fluoride, carbonyl fluoride, and various fluorinated hydrocarbons. The health effects of the gaseous fraction at the concentrations, which occur in the PTFE processing industry, are not clearly known. The ultrafine particles, which are produced in the degradation, have turned out to be the cause of the toxic pulmonary and lethal effects in the experimental animals. These particles probably carry to the lungs small molecular products (e.g. hydrogen fluoride, carbonyl fluoride) and very reactive compounds like free radicals, because their effectiveness strongly depends on the age of the particle. The agents in the degradation products, which cause polymer fume fever, are not known.
The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals 124. Thermal Degradation Products of Polyethylene, Polypropylene, Polystyrene, Polyvinylchloride and Polytetrafluoroethylene in the Processing of Plastics. p. 35 (1998); Available from, as of August 11, 2015: https://www.inchem.org/documents/kemi/kemi/ah1998_12.pdf
It seems that ultrafine particles with a median diameter of approximately 26 nm cause the high pulmonary toxicity and mortality /in animals/. The effects are eliminated if the particles are filtered away from the exposure atmosphere. It has been suggested that particles contain very reactive compounds, e.g. free radicals. If an additional vessel is placed into the degradation product stream between the degradation system and the animals, thus ageing of the particles, the toxicity decreases.
The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals 124. Thermal Degradation Products of Polyethylene, Polypropylene, Polystyrene, Polyvinylchloride and Polytetrafluoroethylene in the Processing of Plastics. p. 35 (1998); Available from, as of August 11, 2015: https://www.inchem.org/documents/kemi/kemi/ah1998_12.pdf
Pet birds are susceptible to developing PTFE toxicosis. Most of these cases have been due to overheated frying pans within the household. At temperatures above 280 C, PTFE-coated surfaces begin to emit degradation products in the form of particulates and gas. Subsequent inhalation of these by-products by birds can result in various clinical signs, including open-beak breathing, chirping, incoordination, lateral recumbency, convulsions, and death. The most common pathologic lesion is severe, extensive, necrotizing and hemorrhagic pneumonitis and edema. The primary mechanism of injury is direct injury of type I pneumocytes and capillary endothelial cells by PTFE degradation products, allowing fluid and blood to leak into the airways. Although PTFE toxicosis has been reported infrequently in humans as 'polymer fume fever,' birds are much more sensitive to inhaled toxicants. This unique sensitivity of birds is due to the anatomy of their respiratory system. Most birds have 9 air sacs (with some species-dependent variations) surrounding the lungs. The lungs are very rigid and do not expand; instead, the air sacs act as a bellows to ventilate the lungs, which are the site of gas exchange. Due to this structural arrangement, airflow within the avian respiratory system is unidirectional. Gas exchange occurs in the lungs as a cross-current system. Specifically, this situation means that air passing through the parabronchi and blood moving through the capillaries travel at right angles to each other. This arrangement allows for very efficient gas exchange as carbon dioxide and oxygen pressure gradients are preserved along the length of the connection between the parabronchus and capillary sytem. However, other gases (for example, PTFE degradation products, carbon monoxide) that are contained in the inhaled air will also be present at increased levels with oxygen. If the gas is toxic, this increased concentration will lead to significant respiratory compromise, resulting in hypoxia and associated hepatic damage.
Shuster KA et al; Comp Med 62 (1): 49-52 (2012)
S-(1,1,2,2-Tetrafluoroethyl)-L-cysteine (TFEC), a major metabolite of the industrial gas tetrafluoroethylene, has been shown to mediate nephrotoxicity by necrosis. TFEC-induced cell death is associated with an early covalent modification of specific intramitochondrial proteins; including aconitase, alpha-ketoglutarate dehydrogenase (KGDH) subunits, HSP60 and HSP70. Previous studies have indicated that the TAMH line accurately models TFEC-induced in vivo cell death with dose- and time-dependent inhibitions of both KGDH and aconitase activities. Here, ... the molecular pathway leading to TFEC-mediated cell death /was shown to be/ associated with an early cytosolic to mitochondrial translocation of BAX, a pro-apoptotic member of the BCL-2 family. Immunoblot analyses indicated movement of BAX (21 kDa) to the mitochondrial fraction after exposure to a cytotoxic concentration of TFEC (250 uM). Subsequent cytochrome c release from mitochondria was also demonstrated, but only a modest increase in caspase activities was observed, suggesting a degeneration of early apoptotic signals into secondary necrosis. Significantly, TAMH cells overexpressing BCL-xL preserved cell viability even to supratoxicological concentrations of TFEC (< or =600 uM), and this cytoprotection was associated with decreased HSP70i upregulation, indicating suppression of TFEC-induced proteotoxicity. Hence, TFEC-induced necrotic cell death in the TAMH cell line is mediated by BAX and antagonized by the anti-apoptotic BCL-2 family member, BCL-xL. / S-(1,1,2,2-Tetrafluoroethyl)-L-cysteine/
PMID:15588723 Ho HK et al; Biochem Pharmacol 69 (1): 147-57 (2005)
Several halogenated alkenes are metabolized in part to cysteine S-conjugates, which are mitochondrial toxicants of kidney and, to a lesser extent, other organs. Toxicity is due to cysteine S-conjugate beta-lyases, which convert the cysteine S-conjugate into pyruvate, ammonia and a reactive sulfur-containing fragment. ... Mitochondrial aspartate aminotransferase and mitochondrial branched-chain aminotransferase exhibit beta-lyase activity toward S-(1,2-dichlorovinyl)-L-cysteine (the cysteine S-conjugate of trichloroethylene) and S -(1,1,2,2-tetrafluoroethyl)-L-cysteine (the cysteine S-conjugate of tetrafluoroethylene). Turnover leads to eventual inactivation of these enzymes. Here /it is reported/ that mitochondrial L-alanine-glyoxylate aminotransferase II, which, in the rat, is most active in kidney, catalyses cysteine S-conjugate beta-lyase reactions with S -(1,1,2,2-tetrafluoroethyl)-L-cysteine, S-(1,2-dichlorovinyl)-L-cysteine and S -(benzothiazolyl-L-cysteine); turnover leads to inactivation. Previous workers showed that the reactive-sulfur-containing fragment released from S-(1,1,2,2-tetrafluoroethyl) L-cysteine and S -(1,2-dichlorovinyl)-L-cysteine is toxic by acting as a thioacylating agent - particularly of lysine residues in nearby proteins. Toxicity, however, may also involve 'self-inactivation' of key enzymes. The present findings suggest that alanine-glyoxylate aminotransferase II may be an important factor in the well-established targeting of rat kidney mitochondria by toxic halogenated cysteine S-conjugates. Previous reports suggest that alanine-glyoxylate aminotransferase II is absent in some humans, but present in others. Alanine-glyoxylate aminotransferase II may contribute to the bioactivation (toxification) of halogenated cysteine S-conjugates in a subset of individuals exposed to halogenated alkenes. / S-(1,1,2,2-Tetrafluoroethyl)-L-cysteine/
PMID:12859250 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1223738 Cooper AJ et al; Biochem J 376 (Pt 1): 169-78 (2003)
Several haloalkenes are metabolized in part to nephrotoxic cysteine S-conjugates; for example, ... tetrafluoroethylene /is/ converted to ... S-(1,1,2,2-tetrafluoroethyl)-L-cysteine (TFEC) ... Most halogenated cysteine S-conjugates are metabolized by cysteine S-conjugate beta-lyases to pyruvate, ammonia, and an alpha-chloroenethiolate or an alpha-difluoroalkylthiolate (with TFEC) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins. Nine mammalian pyridoxal 5'-phosphate (PLP)-containing enzymes catalyze cysteine S-conjugate beta-lyase reactions, including mitochondrial aspartate aminotransferase (mitAspAT), and mitochondrial branched-chain amino acid aminotransferase (BCAT(m)). Most of the cysteine S-conjugate beta-lyases are syncatalytically inactivated. TFEC-induced toxicity is associated with covalent modification of several mitochondrial enzymes of energy metabolism. Interestingly, the alpha-ketoglutarate- and branched-chain alpha-keto acid dehydrogenase complexes (KGDHC and BCDHC), but not the pyruvate dehydrogenase complex (PDHC), are susceptible to inactivation. mitAspAT and BCAT(m) may form metabolons with KGDHC and BCDHC, respectively, but no PLP enzyme is known to associate with PDHC. Consequently, /it was hypothesized/ that not only do these metabolons facilitate substrate channeling, but they also facilitate toxicant channeling, thereby promoting the inactivation of proximate mitochondrial enzymes and the induction of mitochondrial dysfunction. /S-(1,1,2,2-tetrafluoroethyl)-L-cysteine/
PMID:12167474 Cooper AJ et al; Biochem Pharmacol 64 (4): 553-64 (2002)
