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At least 73 records · Page 4Linked to original sources
PubMed1998

"Propylene spaced" allyl tin reagents: a new class of fluorous tin reagents for allylations under radical and metal-catalyzed conditions.

A new generation of propylene-spaced fluorous allyltin reagents [(Rf(CH2)3)3SnCH2CH = CH2] is described. These succeed in radical allylations where their lower homologs (ethylene-spaced) fail, and they provide improved performance in transition metal catalyzed allylations. The reagents and byproducts are readily separated by simple fluorous-organic liquid-liquid or solid-liquid extractions.

Aldehydes↗
PubMed2001

Dichlorobis(4-methylpentan-2-onato-C4,O)tin(IV) and bis(4-methylpentan-2-onato-C4,O)(2-thioxo-1,3-dithiole-4,5-dithiolato-S,S')tin(IV) at 150 K.

The structures of the ketotins determined here, [SnCl(2)(C(6)H(11)O)(2)] and [Sn(C(3)S(5))(C(6)H(11)O)(2)], respectively, along with that previously reported for [MeC(O)CH(2)CMe(2)](2)SnI(2), are compared with the structures of the analogous estertins [MeOC(O)CH(2)CH(2)](2)SnX(2). Pairwise comparison of the mean ketotin [estertin] Sn-X and Sn-O distances as Sn-X 2.4422 (4) [2.4054 (7) A], 2.4970 (4) [2.471 (2) A] and 2.8463 (4) [2.7788 (8) A] and Sn-O 2.4926 (12) [2.528 (1) A], 2.6110 (11) [2.629 (7) A] and 2.435 (3) [2.525 (4) A] (for X = Cl, S and I, respectively) clearly demonstrates the superior donor ability of the ketotin O atom in chelate formation.

Journal Article↗
PubMed1992

Comparative effects of tin- and zinc-protoporphyrin on steroidogenesis: tin-protoporphyrin is a potent inhibitor of cytochrome P-450-dependent activities in the rat adrenals.

Synthetic metalloporphyins inhibit formation of bilirubin by the heme oxygenase system, an ability that is of considerable experimental and clinical interest for suppression of jaundice in the newborn. The present investigation compares the consequences of treatment with Sn- and Zn-protoporphyrin on hemoprotein-dependent enzymes of the rat adrenals and corticosterone production and defines Sn-protoporphyrin as a potent toxin to adrenal functions. Treatment of rats with Sn-protoporphyrin (two doses of 50 mumols/kg, in 7 d) resulted in a marked reduction of 30-40% in cytochrome P-450-dependent adrenal microsomal 21 alpha-hydroxylase and mitochondrial 11 beta-hydroxylase activities. In the serum, the levels of corticosterone were reduced to about 70% of the control value. In addition, the mitochondrial cytochrome P-450SCC activity was decreased by about 50%. This decrease, however, could not be attributed to a reduced total heme level or an accelerated heme degradatory activity. Disruption by Sn-protoporphyrin of adrenal hemoprotein-dependent functions was not restricted to steroidogenic activities and encompassed drug metabolism activity of the organ; benzo(a)pyrene hydroxylase activity of both the microsomal and the mitochondrial fractions, as well as the microsomal NADPH-cytochrome P-450 reductase activity, were significantly reduced. Zn-protoporphyrin did not cause significant alterations in the above measured parameters although it too was effective in inhibiting the hepatic microsomal heme oxygenase activity. In light of the presently defined adverse effects of Sn-protoporphyrin on adrenal steroidogenesis, we suggest Zn-protoporphyrin is the agent of choice for potential use in treatment of hyperbilirubinemia in humans.

Adrenal Glands↗
PubMed2003

Tin in canned food: a review and understanding of occurrence and effect.

Tinplate is light gauge, steel sheet or strip, coated on both sides with commercially pure tin and has been used for well over a hundred years as a robust form of food packaging. Altogether, about 25,000 million food cans are produced and filled in Europe per annum, about 20% of these having plain internal (unlacquered) tin-coated steel bodies. Worldwide, the total for food packaging is approximately 80,000 million cans. Tinplate is also extensively used for the production of beverage cans. Europe produces and fills over 15,000 million tinplate beverage cans per annum all of which are internally lacquered. The use of tinplate for food and beverage packaging, will result in some tin dissolving into the food content, particularly when plain uncoated internal surfaces are used. The Provisional Tolerable Weekly Intake for tin is 14 mg/kg body weight and recommended maximum permissible levels of tin in food are typically 250 mg/kg (200 mg/kg UK) for solid foods and 150 mg/kg for beverages. However, the question arises as to whether evidence exists that such elevated levels of tin in food in any way constitute a risk to human health. This review considers the factors affecting the dissolution of tin, the reported measurements/surveys of actual levels of tin in canned foods and the studies and reports of acute (short term) toxicity relating to the ingestion of elevated levels of tin in food products. Chronic studies are mentioned, but are not covered in detail, since the review is mainly concerned with possible effects from the ingestion of single high doses. From published data, there appears to be a small amount of evidence suggesting that consumption of food or beverages containing tin at concentrations at or below 200 ppm has caused adverse gastrointestinal effects in an unknown but possibly small proportion of those exposed. However, the evidence supporting this assertion is derived from reports of adverse effects which offer data that are limited, incomplete or of uncertain veracity. Clinical studies provide greater confidence regarding the effects of exposure concentration and dose, but few relevant studies have been made. Adverse gastrointestinal effects were observed in limited clinical studies at concentrations of 700 ppm or above, although no adverse gastrointestinal effects were also reported in two studies at higher concentrations. Overall, therefore, the published data do not present a particularly comprehensive profile on the toxic hazard to man of acute exposure to divalent inorganic tin. A food survey suggested that the contents of almost 4% of plain internal tinplate food cans contain over 150 mg/kg of tin and over 2.5 million such cans are consumed every year in the UK alone. Despite this, in the last 25 years, there have been no reports of acute effects attributable to tin contamination in the range 100-200 ppm. These facts strongly suggest that there is little evidence for an association between the consumption of food containing tin at concentrations up to 200 ppm and significant acute adverse gastrointestinal effects. Clearly though, only further clinical studies will generate unequivocal evidence that current legislative limits provide safe levels for adults in the general population.

Animals↗
PubMed1988

Toxicity of tin and its compounds.

Inorganic tin salts are poorly absorbed and rapidly excreted in the faeces; as a result they have a low toxicity. Only about 5 per cent is absorbed from the gastrointestinal tract, widely distributed in the body, then excreted by the kidney. Some tin is deposited in lung and bone. Some tin salts can cause renal necrosis after parenteral doses. Mutagenic studies on metallic tin and its compounds have been negative. Long-term animal carcinogenic studies have shown fewer malignant tumours in animals exposed to tin than in controls. Human volunteers developed mild signs of toxicity with tin, given in fruit juices, at a concentration of 1400 mg per litre. The WHO 1973 permissible limit for tin in tinned food is 250 micrograms per kg. The adult daily intake of tin was about 17 mg per day in 1940, but it has now decreased to about 3.5 mg, due to improvements in technique of tinning with enamel overcoat and crimped lids to minimize exposure to tin and lead solder. This level is well below the level of 5-7 mg per kg body weight shown to give rise to toxic symptoms. Tin deficiency has not been described in man. Amounts in excess of 130 mg per day have been shown to accumulate in liver and kidneys. Many of the organotin compounds are toxic; the most toxic being trimethyltin and triethyltin, which are well absorbed from the gastrointestinal tract. Most of the other alkyl and aryltin compounds are poorly absorbed from the gastrointestinal tract, and are therefore less toxic when given orally than when given parenterally. The main results of toxicity are skin and eye irritation; cholangitis of the lower biliary tract, and later hepatotoxicity; and neurotoxicity, which has been shown to be due to intramyelin oedema induced by triethyltin, and neuronal necrosis caused by trimethyltin. Many of the organotin compounds affect mitochondrial oxidative phosphorylation and alter membranes, but the contribution of these biochemical and membrane effects in the cause of intramyelin oedema and neuronal necrosis has not been fully clarified. Widespread degeneration results, especially with trimethyltin. Peripheral neuropathy has not been reported as occurring with either inorganic or organic tin in humans. Certain dialkyltin compounds have been shown to cause adverse effects on cell-mediated immunity, specifically on the T cell lymphocyte. Experimental studies have failed to reveal any evidence of carcinogenicity, mutagenicity, or teratogenicity. Recent studies suggest that tin compounds exhibit some antitumour activity and may have a future role in cancer diagnosis and chemotherapy, and in controlling hyperbilirubinaemia.

Animals↗