SEARCH · PubMed Health

Results for “IOPANOIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources

PubMed1978

Nutritionally-induced alterations in thyroid hormone metabolism and thermogenesis.

Serum 3,5,3'-triiodothyronine (T3) is increased by overnutrition and decreased by starvation. The production rate of T3 was increased by overfeeding (82%), but T4 production did not change. Feeding a weight maintenance diet with high CHO mimiced serum T3 and rT3 changes of overfeeding, substitution of CHO by FAT those of starvation. VO2 increased during overfeeding and in T4 equilibrated volunteers supplemented with 40 microgram T3 daily for 2 weeks. No weight change occurred in the latter subjects. Yet no decrease in VO2 was found when serum T3 was reduced by the administration of iopanoic acid. VO2 decreased during starvation in normal and hypothyroid rats, and in hypothyroid animals replaced with T4 or T3.

Animals↗

PubMed1978

Clinical aspects of drug-induced hepatitis.

The drug reactions of the liver may be classified as to (1) reproducibility, (2) severity, (3) localization and (4) duration of the lesion. Ad 1) Few drugs give a reproducible, dose dependent, hepatic reaction (e.g. acetaminophen), a greater problem is the unpredictable, dose independent reactions caused by "indirect" hepatotoxic drugs (e.g. imipramin). Ad 2) Drug reactions may be fatal (e.g. halothane), of limited clinical importance (e.g. clorpromazin) or clinically insignificant (e.g. iopanoic acid). Ad 3) Histologically, and to some extent clinically, hepatocellular (e.g. propylthiouracil) may be distinguished from cholestatic (e.g. tolbutamide) reactions, but overlapping (e.g. phenylbutazone) and individual variations are common. Ad 4) Most drug reactions are acute, but an insiduous course, developping to cirrhosis, is increasingly recognized (e.g. oxyphenacetin). Drug reactions are usually not clinically, biochemically and morphologically distinct from other common liver diseases and are only diagnosed if this possibility is constantly kept in mind. Treatment other than withdrawal of suspected or known etiologic agents is virtually lacking. The basis for prophylaxis is careful registration of all drug reactions. Potentially hepatotoxic drugs should only be administered after thorough cost/benefit considerations.

Chemical and Drug Induced Liver Injury↗

PubMed1980

Thyroid, renal, and hepatic function tests following cholecystography with high-dose contrast agents.

Serum biochemical tests were observed for about three weeks following oral cholecystography with fractionated high doses (6 g) of iopanoic acid (Telepaque) or sodium ipodate (Biloptin) in 24 and 29 patients, respectively. Both agents produced similar effects. No significant changes were seen in renal or hepatic function except for a mild increase in bilirubin on day 22. Serum urate decreased 10% on day 4, but the change was not significant. On days 4 and 11, there were significant increases in thyroid-stimulating hormone, thyroxine and free thyroxine index, and a moderate fall in triiodothyronine. Reverse triiodothyronine increased sharply on day 4. The pattern of changes observed suggests that these contrasts interfere with the extrathyroidal deiodination of iodothyronines. The temporary rise in thyroxine and free thyroxine index exceeded reference ranges in about half of all subjects, but they remained clinically euthyroid. Thyroid function tests should be interpreted with caution within three weeks of cholecystography.

Adult↗

PubMedDate not supplied

Iodothyronine and thyrotropin concentrations after iodoamide administration for angiographic studies.

In order to study the effect of iodoamide (a contrast medium widely used for urographic and arteriographic studies) on thyroid function, seventeen subjects were studied before and after arteriographic examinations employing this contrast compound. Serum concentrations of T4, T3, rT3 and TSH were not modified during the observation period by the administration of iodoamide. This finding is in contrast with the observation that iopanoic acid and ipodate, used for cholecystographic examinations, can reduce the serum concentrations of T4 and T3 with a concomitant increase in rT3. Therefore, iodoamide is not useful in the treatment of hyperthyroidism.

Adult↗

PubMed1994

Thyrotoxicosis factitia in a post-aortocoronary bypass patient.

A 52-yr-old man presented with an evolving myocardial infarction and unstable angina. Previously, he had undergone aortocoronary bypass surgery for triple vessel disease and at that time was diagnosed as hypothyroid. He had been refractory to thyroxine treatment and now required 0.3 mg thyroxine daily. On admission, he was hypertensive, tachycardic and found to be thyrotoxic secondary to excess thyroid hormone ingestion. Treatment with iopanoic acid was started. Despite medical therapy he continued to have unstable angina. Coronary angiography confirmed further triple vessel disease with blockage to his previous grafts. He was taken to surgery for coronary revascularization. On arriving in the intensive care unit he developed a thyroid storm. His temperature increased from 36.5 to 39.5 degrees C requiring a cooling blanket and cold irrigation down a nasogastric tube. An esmolol infusion was started to control his persistent tachycardia but this depressed his myocardial contractility. He required amrinone and noradrenaline infusions as further inotropic support. For sedation and muscle relaxation, intravenous propofol infusion and doxacurium were given. Over the following 20 hr the patient's condition stabilized. In conclusion, we describe the use of a short-acting beta blocker to avoid compromising an impaired myocardium during a thyroid storm which we could stop if the patient's cardiac condition deteriorated. In addition, amrinone, a phosphodiesterase inhibitor, was our inotrope of choice as it does not act on the already blocked beta adrenergic system.

Adrenergic beta-Antagonists↗

PubMed1982

One enzyme for the 5'-deiodination of 3,3',5'-triiodothyronine and 3',5'-diiodothyronine in rat liver.

Many studies suggest that one enzyme is involved in the phenolic ring deiodination of iodothyronines in rat liver and kidney and another one in the tyrosyl ring deiodination. This study describes some characteristic of the phenolic ring (5'-) deiodination of rT3 and 3',5'-T2 by rat liver microsomes. At pH 7.2 the Km values of the 5'-deiodination of rT3 and 3',5'-T2 were 0.103 and 0.77 microM, respectively. 3',5'-T2 and rT3 inhibited the respective 5'-deiodination reactions competitively, the Ki values being 1.05 and 0.134 microM, respectively. Several radiographic contrast agents markedly inhibit the 5'-monodeiodination or rT3 and 3',5'-T2, the type of inhibition being competitive. Of these compounds iopanoic acid, ipodic acid and iophenoxic acid are the most potent inhibitors with Ki values of approximately 2 microM for both reactions. The non-iodine containing compound 8-anilino-1-naphthalene sulphonic acid (ANS) appeared to be a very strong competitive inhibitor of both 5'-deiodinations (Ki 4.3-4.7 microM), whereas salicylic acid, which as ANS inhibits the binding of iodothyronines to T4-binding globulin, inhibited these reactions to a much lesser extent (Ki 300-500 microM). On the other hand, diiodosalicylic acid was a very strong inhibitor. The beta-adrenergic blocker D,L-propranolol was a weak noncompetitive inhibitor of both 5'-deiodinations (Ki 0.4-0.7 mM). These reactions were also inhibited by various 2,6-diiodophenol derivatives, triiodophenol being the strongest and diiodotyrosine the weakest inhibitor tested. Comparing the Ki values of various inhibitors for the 5'-deiodination of rT3 and 3',5'-T2, a positive correlation between these values was found (r = 0.97). It was concluded that rT3 (to 3,3'-T2) and 3'-5'-T2 (to 3'-T1) monodeiodinating activities are very similar to each other and that there may just be one monodeiodinase catalyzing the 5'-deiodination of iodothyronines in rat liver.

Anilino Naphthalenesulfonates↗

PubMed1985

Thyroid hormone metabolism in primary cultures of fetal rat brain cells.

The metabolism of thyroxine 3,5,3',5'-tetraiodothyronine, (T4) and 3,5,3'-triiodothyronine (T3) was studied in primary cultures of dispersed fetal rat brain cells. Cultured brain cells actively metabolized both T4 and T3 by enzyme catalyzed deiodination reactions which increase (type II 5'-deiodinase) or decrease (type I 5'-deiodinase and type III 5-deiodinase) the bioactivity of thyroid hormone. Homogenates of cultured brain cells showed both type I and type II 5'-deiodinating activities and these two enzymes tended to differ in their time course of appearance. Cultures exposed to 10 microM cytosine arabinoside for 16 h showed up to a 70% reduction in type I activity without decreasing the type II enzyme suggesting that the type II enzyme is associated with non-dividing neuronal cells. The predominant pathway for T4 and T3 metabolism in situ was tyrosyl-ring or type III 5'-deiodination which followed first order kinetics with a t1/2 of 70 min. T4 to T3 conversion by the type II enzyme was consistently observed after correcting for the degradation of newly formed T3 by the type III enzyme. In situ, both type II and type II enzymes were thiol-dependent and both activities were inhibited by iopanoic acid. Type III 5-deiodination of T4 produced 34 fmol 3,3,5'-triiodothyronine (rT3)/h per 10(6) cells at 10 mM dithiothreitol (DTT) and 97 fmol of rT3/h per 10(6) cells at 50 mM DTT. T3 production by the type II enzyme was 1.2 and 4.4 fmol of T3/h per 10(6) cells at 10 and 50 mM DTT, respectively. Thyroid hormone deficient culture conditions increased type II enzyme activity by 4-5-fold within 48 h and this was prevented in a dose-dependent fashion by supplementing the media with increasing amounts of T3. These data indicate that primary cultures of dispersed brain cells mimic the intact cerebral cortex with respect to the metabolism of thyroid hormone and the regulatory mechanisms which defend cerebrocortical T3 levels. The vigorous metabolism of both T4 and T3 by these cultures may explain some of the difficulties in demonstrating thyroid hormone-dependent biochemical changes at physiologically relevant levels of thyroid hormone.

Animals↗

PubMed1994

Expression of type II thyroxine 5'-deiodinase from rat harderian gland in Xenopus laevis oocytes.

The presence of isoenzymes mediating the conversion of thyroxine to 3,5,3'-triiodothyronine has been studied according to characteristic kinetics and physiological regulation. In this paper, we report the expression of type II 5'-deiodinase (5'D) activity in oocytes of Xenopus laevis. Oocytes injected with total RNA extracted from rat Harderian gland, and then incubated up to five days demonstrated a progressive increase in 5'D activity, reaching a maximal value at 24 h; then, 5'D activity remained almost stable for an additional period of four days. Characteristics of the enzyme activity expressed by oocytes included its inhibition by iopanoic acid, but not by propylthiouracil, and its increase during beta-adrenergic agonist treatment and hypothyroidism. The expressed activity manifests characteristics typical of the type II isoenzyme. Deiodinating activity in oocytes also exhibited diurnal variations. In this study, 5'D activity expressed in oocytes exhibited low values when animals were killed during the day, and high values when animals were killed at night. Maximal values were reached 3-4 h before the nocturnal peak of 5'D activity in Harderian gland crude homogenates. Results suggest that the in vivo activation of 5'D by isoproterenol, hypothyroidism, or dark exposure may be caused by an increase in the synthesis and/or maturation of the RNA expressing the enzyme.

Animals↗

PubMed1976

Pharmacology and physiology of the biliary radiographic contrast materials.

(1) Solubilization of Telepaque in the intestine is a limiting factor in the rate of intestinal absorption. Bilopaque and Oragrafin are more water-soluble and appear to be better absorbed than Telepaque. (2) Bile salts in the intestinal lumen increase the solubility of Telepaque. Therefore, a fatty meal administered with the Telepaque is desirable to evacuate bile salts from the gallbladder into the intestine. This is not required for the more water-soluble agents, Biopaque and Oragrafin. (3) The degree of protein binding of the contrast agents can be related to the degree of toxicity. Cholografin is the most highly bound and is the most toxic. (4) Hepatic receptor proteins may specifically bind the biliary contrast agents. This may be the reason that the renal contrast materials are poorly escreted in bile compared to the biliary contrast agents. (5) Telepaque is conjugated in the liver with glucuronide making the compound more soluble in bile. This prevents precipitation of Telepaque in the gallbladder and avoids reabsorpiton from the intestine. (6) The biliary excretion of Telepaque is facilitated by bile salts. Therefore, the administration of a fatty meal with Telepaque not only increases the rate of intestinal absorption of Telepaque but also the rate of biliary excretion. (7) The rate of biliary excretion of both the oral and the intravenous contrast agents appears to be limited by a hepatic transport maximum. Above a certain dose, increased amounts of the contrast agents do not result in more rapid excretion of the agents into bile. Rapid infusion of intravenous contrast agents results in high plasma concentration and greater urinary excretion, without increasing the biliary excretion. It does not appear to be indicated in clinical practice. (8) The biliary concentration of the contrast agents used for intravenous cholangiography is determined by their rate of biliary excretion, the choleretic effect of the contrast agent, and factors that determine the rate of basal bile flow. Fixed coupling of water with the biliary excretion of these contrast agents imposes an inherent limitation on the concentration of the contrast agent in bile. It appears that the biliary concentration of the intravenous contrast materials can be increased by having the patient fast prior to intravenous cholangiography. This decreases the enterohepatic circulation of bile salts and the rate of bile-salt-dependent bile flow. (9) Failure of the gallbladder to visualize after administration of Telepaque when there is adequate biliary excretion may be due to cystic duct obstruction, failure of the inflamed gallbladder mucosa to reabosrb water, or reabsorption or the contrast agent by the diseased gallbladder mucosa. (10) Maximum concentration of Telepaque occurs at 14-19 hr after ingestion. It is at this time that radiographs of the gallbladder should be made. With Bilopaque, peak concentration occurs at 10 hr so radiographs can be made earlier when Bilopaque is used.

Animals↗

PubMed1986

Avian hepatic T3 generation by 5'-monodeiodination: characterization of two enzymatic pathways and the effects of goitrogens.

The enzymatic nature of 5'-monodeiodination (5'-D) in avian liver homogenates was demonstrated by abolishment of activity by iopanoic acid (IOP). T3 production from T4 was dependent on enzyme and substrate concentrations, incubation time, incubation temperature, and pH. Two pathways of 5'-D activity were present in avian liver and exhibited characteristics similar to those described in mammalian tissues. Type II activity was identified as propylthiouracil (PTU)-insensitive activity. Type I (PTU-sensitive) was determined by difference between Total and Type II. Km values were 1.58 microM T4 for Total activity and 0.90 nM T4 for Type II, corresponding to the characteristics of the mammalian pathways. The effects of goitrogens on avian hepatic 5'-D were equivalent to those reported for the mammalian enzyme.

Animals↗

PubMed1992

Pathophysiology of chemical injury of the thyroid gland.

Many goitrogenic xenobiotics that increase the incidence of thyroid tumors in rodents exert a direct effect on the thyroid gland to disrupt one of several possible steps in the biosynthesis and secretion of thyroid hormones. This includes: (1) inhibition of the iodine trapping mechanism (thiocyanate or perchlorate); (2) blockage of organic binding of iodine and coupling of iodothyronines to form thyroxine (T4) and triiodothyronine (T3) (e.g. sulfonamides, thiourea, methimazole, and aminotriazole, amongst others); (3) inhibition of thyroid hormone secretion by an effect on proteolysis of active hormone from the colloid (lithium or an excess of iodide). Another large group of goitrogenic chemicals disrupts thyroid hormone economy by increasing the peripheral metabolism of thyroid hormones through an induction of hepatic microsomal enzymes. This group includes CNS-acting drugs (phenobarbital, benzodiazepines), calcium channel blockers (nicardipine, nifedipine), steroids (spironolactone), retinoids, chlorinated hydrocarbons (chlordane, DDT, TCDD), polyhalogenated biphenyls (PCB, PBB), and enzyme inducers. Thyroid hormone economy also can be disrupted by xenobiotics that inhibit the 5'-monodeiodinase which converts T4 in peripheral sites (e.g. liver and kidney) to biologically active T3. Inhibition of this enzyme by FD&C Red No. 3, amiodarone, and iopanoic acid lowers circulating T3 levels which results in a compensatory increased secretion of thyroid stimulating hormone (TSH), follicular cell hypertrophy and hyperplasia, and an increased incidence of follicular cell tumors in 2-year or lifetime studies in rats. Physiologic perturbations alone, such as the feeding of an iodine-deficient diet, partial thyroidectomy, natural goitrogens in certain foods, and transplantation of TSH-secreting pituitary tumors in rodents also can disrupt thyroid hormone economy and, if sustained, increase the development of thyroid tumors in rats. A consistent finding with all of these goitrogens, be they either physiologic perturbations or xenobiotics, is the chronic hypersecretion of TSH which places the rodent thyroid gland at greater risk to develop tumors through a secondary mechanism of thyroid oncogenesis.

Animals↗

PubMed2003

Light-induced hormone conversion of T4 to T3 regulates photoperiodic response of gonads in birds.

Reproduction of many temperate zone birds is under photoperiodic control. The Japanese quail is an excellent model for studying the mechanism of photoperiodic time measurement because of its distinct and marked response to changing photoperiods. Studies on this animal have suggested that the mediobasal hypothalamus (MBH) is an important centre controlling photoperiodic time measurement. Here we report that expression in the MBH of the gene encoding type 2 iodothyronine deiodinase (Dio2), which catalyses the intracellular deiodination of thyroxine (T4) prohormone to the active 3,5,3'-triiodothyronine (T3), is induced by light in Japanese quail. Intracerebroventricular administration of T3 mimics the photoperiodic response, whereas the Dio2 inhibitor iopanoic acid prevents gonadal growth. These findings demonstrate that light-induced Dio2 expression in the MBH may be involved in the photoperiodic response of gonads in Japanese quail.

Animals↗

PubMed1983

Thyroxine action on the rat liver nuclear thyroid-hormone receptors. Binding of thyroxine to the nuclear non-histone protein and induction of mitochondrial alpha-glycerophosphate dehydrogenase activity.

The possibility that thyroxine (T4) itself exerts the hormonal effect in vivo on the rat liver nuclear receptor was studied with the aid of iopanoic acid (IOP), an inhibitor of the conversion of T4 into tri-iodothyronine (T3). After administration of 2.4 micrograms of T4/100 g body weight to hypothyroid rats for 7 days, T4 and T3 concentrations in serum and in the liver nuclear non-histone protein (NHP) were all increased to the hyperthyroid range. Hepatic mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) activity and DNA content increased significantly. The equilibrium association constant (Ka) of the nuclear T3 receptor was unchanged and the maximal binding capacity (Cmax.) increased 1.4-fold. Simultaneous administration of IOP (5 mg/100 g body weight) to the rats given 2.4 micrograms of T4/100 g body weight completely blocked the conversion into T3. The serum T4 was even more increased, whereas the serum T3 decreased to the hypothyroid range. Although the NHP-bound T4 was at a concentration comparable with the rats given T4 alone, no NHP-bound T3 was detected. Yet the alpha-GPD activity was elevated 2.8-fold and the DNA content increased to the same extent as observed in the rats given T4 alone. The Ka and Cmax. of the nuclear receptor were significantly decreased. After administration of 48 or 480 micrograms of T4/100 g body weight for 3 days, serum T4 and T3 were markedly increased. The NHP-bound T3 was also increased, but no NHP-bound T4 was detected. The alpha-GPD activity was markedly elevated, but the DNA content was unchanged. The Cmax. per g of liver was increased, whereas the Ka remained unchanged. Simultaneous administration of IOP to these animals could not completely block the T4 conversion. The observed hormonal effects in the absence of nuclear T3 indicate that T4 possesses the intrinsic hormonal activities on the rat liver. T4 is less potent in induction of alpha-GPD activity but as potent in increment of hepatic DNA as T3. Although the binding site for T4 is not fully characterized, it appears to be acidic NHP. T4 is an active hormone, yet is also a prohormone of T3, offering the closest analogy with testosterone.

Animals↗

PubMed2002

Tissue-specific regulation of type III iodothyronine 5-deiodinase gene expression mediates the effects of prolactin and growth hormone in Xenopus metamorphosis.

Prolactin (PRL) and growth hormone (GH) are known to be able to act as antimetamorphic hormones. From investigations of how PRL inhibits Xenopus tail regression in vitro, it was found that the both hormones could, in addition to their known antimetamorphic actions, upregulate mRNA expression of type III iodothyronine 5-deiodinase (5D), an enzyme that inactivates thyroid hormones (TH). Conversely, both PRL and GH were found to downregulate 5D mRNA expression in the liver. Blockage by PRL of TH-induced tail regression in organ culture was released by treatment with iopanoic acid (IOP, an inhibitor of 5D activity). The IOP-released tail regression displayed a unique morphology of the larger fins retained on the regressing tails, consistent with the finding that mRNA for both PRL receptor and 5D were enriched in the fin. The results suggest that the metamorphosis-modulating actions of PRL and GH are mediated, at least partially, by tissue-specific regulation of 5D mRNA expression.

Animals↗

PubMed2001

The use of oral radiographic contrast agents in the management of hyperthyroidism.

Oral iodinated radiographic contrast agents such as ipodate and iopanoic acid form an important part of the armamentarium used to treat hyperthyroidism. They rapidly and dramatically reduce serum triiodothyronine (T3) levels by inhibiting conversion of thyroxine (T4) to T3 in the periphery and by blocking secretion from the thyroid. Potential risks from the large iodine load resulting from their use limit their widespread applicability. In addition, they are ineffective when used alone on a long-term basis. However, these agents may be especially useful in treating thyrotoxic patients preoperatively, in neonatal Graves' disease, in massive levothyroxine ingestion, and when other conventional antithyroid drugs are unsuccessful or contraindicated.

Administration, Oral↗

PubMed2003

Is there a place for thyroidectomy in older patients with thyrotoxic storm and cardiorespiratory failure?

Early thyroidectomy is the treatment of choice for thyrotoxic storm in patients with thyroid autonomy often induced by iodine. However, older patients who are mostly affected by this condition often have underlying chronic cardiopulmonary diseases, apparently contradicting surgical intervention. The published evidence for suitable treatment strategies in these patients is limited. We report the outcome of a series of older critically ill patients who were treated by thyroidectomy because of thyrotoxic storm. We retrospectively analyzed the outcome of 10 patients (4 males, 6 females; 70 years of age, range, 54-79, Burch-Wartofsky point scale, 61; range, 40-85) with thyrotoxic storm, thyroid autonomy, and severe cardiorespiratory and renal failure with cardiac arrhythmia, coronary artery or chronic obstructive pulmonary disease, or acute inflammation. Thyroidectomy was performed for the following reasons: symptoms of thyrotoxic storm deteriorated or did not improve within 24-48 hours despite intensive medical treatment, or patients developed thionamide-induced agranulocytosis or severe thrombocytopenia. All patients with severe accompanying diseases survived thyroidectomy (early post-operative mortality, 0%). The two oldest patients died 2-3 weeks after thyroidectomy because of myocardial infarction or respiratory failure (late postoperative mortality, 20%). In contrast, in the few previous reports of patients who underwent thyroidectomy for thyrotoxic storm and severe accompanying diseases (n = 7), late postoperative mortality was 43%. The overall mortality for all reported patients including our own, who underwent thyroidectomy for thyrotoxic storm with and without severe accompanying disease (n = 49) was 10%. Our results suggest that early total thyroidectomy should be considered as the method of choice for older, chronically ill patients with thyrotoxic storm complicated by cardiorespiratory and renal failure, especially if high-dose thionamide treatment, iopanoic acid, glucocorticoids, and intensive care fail to improve the patient's conditions within 12-24 hours.

Aged↗

PubMed2000

Excess iodine induces apoptosis in the thyroid of goitrogen-pretreated rats in vivo.

Previously, we observed that excess iodide rapidly suppressed the elevated ornithine decarboxylase activity in the thyroid of propylthiouracil (PTU)-pretreated rats. Excess iodide also induces involution of goitrous thyroids. These findings led us to study effects of excess iodide on apoptosis of rat thyroids. When given to PTU-pretreated rats, excess potassium iodide (KI) (13 mg/kg body weight, 10 mg as iodine) induced DNA fragmentation in the thyroid at the first 3 hours after its treatment. The percentage of DNA fragmentation was also maximal at 3 hours after KI treatment. In methimazole-pretreated rats, the kinetic of DNA fragmentation was nearly the same; apoptosis increased for the first 6 hours and then decreased at 12 hours after KI administration. Other iodinated compounds such as amiodarone and diiodotyrosine have also shown apoptosis-inducing activity, but their effect was observed later than KI. Iopanoic acid had no such effect. Apoptotic changes were also observed with the use of flow cytometry. PTU or methimazole alone had some stimulatory effect on thyroid apoptosis. Iodine effect was not observed in rats treated with either perchlorate or thiocyanate. These results suggest that excess iodine induces thyroid involution in goitrogen-treated rats at least partially by apoptosis.

Amiodarone↗

PubMedDate not supplied

The determination of commonly used iodinated contrast media in postmortem samples using HPLC and TLC.

A rapid micro method is described for the determination of diatrizoic, iothalamic, ioxaglic, and iopanoic acids in postmortem liver and blood. The compounds were extracted with methanol and analyzed by high performance liquid chromatography using a C18 column. The mobile phase consisted of methanol:PIC A with ultraviolet detection at 232 and 242 nm. Recoveries of about 85% were obtained. A thin layer chromatographic system is described which separates the four compounds. The spots were hydrolyzed and sprayed with a diazonium coupling reagent to produce colored spots with sensitivities of 0.02 to 0.1 micrograms. Postmortem levels are given for two deaths involving diatrizoic acid.

Chromatography, High Pressure Liquid↗