Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ISOLATION PERFUSION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 1,387 records · Page 77Linked to original sources
PubMed1976

Synthesis of bile acid monosulphates by the isolated perfused rat kidney.

Perfusion of an isolated rat kidney with labelled bile acids, in a protein-free medium, resulted in the urinary excretion of the labelled bile acid, 3% being converted into polar metabolities in 1h. These metabolities were neither glycine nor taurine conjugates, nor bile acid glucuronides, and on solovolysis yielded the free bile acid. On t.l.c. the metabolite of [24-14C]lithocholic acid had the mobility of lithocholate 3-sulphate. The principal metabolite of [24-14C]chenodeoxycholic acid had the mobility of chenodeoxycholate 7-sulphate; trace amounts appeared as chenodeoxycholate 3-sulphate. [35S]sulphate was incorporated in chenodeoxycholic acid by the kidney, resulting in a similar pattern of sulphation. No disulphate salt of chenodeoxycholic acid was detected. These findings lend support to the hypothesis that renal synthesis may account for some of the bile acid sulphates present in urine in the cholestatic syndrome in man.

Animals↗
PubMed1975

Glucagon and insulin control of gluconeogenesis in the perfused isolated rat liver. Effects on cellular metabolite distribution.

The metabolic effects of glucagon and glucagon plus insulin on the isolated rat livers perfused with 10 mM sodium L-lactate as substrate were studied. Glucagon stimulated gluconeogenesis, ketogenesis and ureogenesis at the concentration used of 2.1 nM. The addition of insulin to give a glucagon-to-insulin ratio of 0.2 reversed all the glucagon effects. The glucagon enhancement of gluconeogenesis was accompanied by a rise in cytosolic and mitochondrial state of reduction of the NAD system and a fall in the [ATP]/[ADP] ratio. The analysis of the intermediary metabolite concentrations suggested, as possible sites of glucagon action, the steps between pyruvate and phosphoenolpyruvate as well as the reactions catalyzed by phosphofructokinase and/or fructose bisphosphatase. All the changes in metabolite contents were abolished when insulin was present. Glucagon increased the intramitochondrial concentration of all the metabolites, whose intracellular distribution was calculated. The finding of a significant rise in the calculated intramitochondrial concentration of oxaloacetate points to pyruvate carboxylation as an important site of glucagon interaction with the gluconeogenic pathway. A primary event in the glucagon action redistributing intracellular metabolites seems to be the mitochondrial entry of malate. The possibility is discussed that the changes in metabolite cellular distribution were brought about by the increased cellular state of reduction caused by the hormone.

Animals↗
PubMed1985

Hepatotoxicity of hornet's venom sac extract in isolated perfused rat liver.

The changes in the activity of some enzymes in parenchymal liver cells were measured in the perfusate of rat isolated liver after a single envenomation with two different doses of Hornet's (Vespa orientalis) venom sac extract (VSE). The maximal observed enzymatic changes were significant: twenty four fold rise of alkaline phosphatase E.C.3.1.3.1(ALP), six fold rise of alanine aminotransferase E.C.2.6.1.2. (ALT) and nine fold rise of aspartate aminotransferase E.C.2.6.1.1. (AST) activity. There were moderate changes (four fold) in lactic dehydrogenase activity E.C.1.1.1.2.7. (LDH) and a non-significant change in gamma-glutamyl-transferase E.C.2.3.2.1. (GGT) activity. These changes varied with the venom's dose. Also a decrease in the rate of effluent draining out via the hepatic vein was noted as an additional sign of liver damage. In light of the biochemical evidence presented here, as well as in previous work, it seems that no further biochemical proof is needed to establish the hepatotoxicity of VSE in rats, cats and probably humans too. It seems that VSE is a predictable hepatotoxin causing a pattern of enzyme changes of the cholangiocellular type.

Alanine Transaminase↗
PubMed1987

Phenylphosphonate: a 31P-NMR indicator of extracellular pH and volume in the isolated perfused rabbit bladder.

31P-NMR has been used extensively to estimate intracellular pH. It also can be used to measure extracellular pH and volume when an NMR-detectable extracellular phosphorous probe is used. Phosphonic acids have been suggested as useful 31P-NMR extracellular markers. The present study was designed to assess the utility of phenylphosphonic acid (PPA) as a 31P-NMR extracellular marker in perfused smooth muscle. Rabbit bladder strips were exposed to PPA concentrations of 1-20 mM. Tension development in response to maximal carbachol challenges (10 microM) was independent of PPA concentration. Addition of PPA (6 mM) to the perfusate supplying the isolated resting rabbit bladder had no effect on 31P-NMR-detectable phosphatic compounds. PPA's resonance frequency was distinctly downfield from endogenous phosphates and demonstrated a pH-dependent chemical shift of +/- 1.12 ppm/pH unit over the range of 6.4 to 7.6 with a pK' of 7.09 at 23 degrees C. The time courses for washing PPA in and out of the resting bladder were best described by monotonic exponential growth (r = 0.972; n = 3) and decay (r = 0.972; n = 3) equations, respectively. Rate and time constants for PPA wash-in (0.039 +/- 0.004 min-1 and 25.7 +/- 2.3 minutes) and washout (0.038 +/- 0.000 min-1 and 26.3 +/- 0.0 minutes) were not significantly different. Using steady state PPA and ATP peak intensities and concentrations, an extracellular-to-intracellular ratio was calculated to be 0.31 +/- 0.03 (n = 3). These data indicate that PPA remains distributed exclusively in the extracellular spaces.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

6-Aminochrysene kinetics in isolated perfused liver.

1. New quantitative assays of 6-aminochrysene by spectrophotometric and g.l.c. methods and t.l.c. separation systems are described. 2. The decline in blood levels of the antitumoral agent 6-aminochrysene was due to its distribution rather than to metabolism to polar metabolites, during liver perfusion experiments. 3. No marked changes in kinetics of 6-aminochrysene were observed during perfusion of livers isolated both from normal and from Walker 256 carcinosarcoma-bearing rats.

Animals↗
PubMed1980

Effects of glucagon, secretin, and vasoactive intestinal polypeptide on gastric somatostatin and gastrin release from isolated perfused rat stomach.

To investigate the role of gastric somatostatin on gastrin secretion, glucagon, secretin, and vasoactive intestinal polypeptide (VIP) were perfused in the isolated pancreas-spleen-duodenum deprived preparation of rat stomach. After a preperfusion with 4.6% dextran Krebs-Ringer bicarbonate buffer containing 5.5 mM glucose, glucagon, secretin, and VIP at the concentrations of 10(-8), 10(-7), and 10(-6) M were infused into the left gastric artery at a constant flow of 2 ml/min for 15 min. All glucagon, secretin, and VIP evoked dose-dependent increases of somatostatin secretion with a simultaneous dose-related decrease of gastrin release. Furthermore, a significant correlation was found between the increase of somatostatin release and the decrease of gastrin secretion induced by glucagon, secretin, and VIP. These results raise the possibility that the suppression of gastrin secretion induced by glucagon, secretin, and VIP may, at least in part, be mediated by local action of gastric somatostatin.

Animals↗
PubMedDate not supplied

Pulmonary elimination and metabolism of 5-fluoro-2'-deoxyuridine in isolated perfused rat lung and lung slices.

Elimination kinetics and metabolism of the cytostatic drug 5-fluoro-2'-deoxyuridine (FUDR) were studied in isolated perfused rat lung and in incubated lung slices. The intact organ exhibited a low clearance of 0.2 to 0.8 ml/min and a calculated first-pass extraction of 2 to 7% of the drug inflow. Thus, the pulmonary uptake of the fluorinated nucleoside from the circulation is low. Within 120 min of perfusion, however, 30 to 45% of the initial FUDR dose was metabolized by the isolated rat lung. The nucleobase metabolite 5-fluorouracil (FU) represented almost all FUDR metabolites in the medium, indicating that this metabolic pathway, mediated by thymidine phosphorylase, is active in lung while the enzymic activity for further pyrimidine degradation is low. This was demonstrated in incubated lung slices, which have a high capacity to transform FUDR into FU, comprising 83 to 95% of the metabolites in the medium. The final catabolic metabolite, alpha-fluoro-beta-alanine, was present in trace amounts only. It is concluded that the pulmonary tissue contains a marked "intrinsic" capacity to transform FUDR into FU, while the metabolic activity for catabolism of the nucleobase metabolites FU and 5,6-dihydrouracil is virtually lacking.

Animals↗
PubMed1976

Effect of histamine and antihistamines on renal hemodynamics and functions in the isolated perfused canine kidney.

Histamine was infused intra-arterially (10-40 mug/min) into isolated blood perfused canine kidneys while functional and hemodynamic parameters were monitored. When perfusion pressure (PP) was kept constant during the infusion of histamine, renal blood flow (RBF) increased from 137 +/- 9 to 181 +/- 9 ml/min (P less than .001). A greater increase in RBF occurred to the inner renal cortex than the outer renal cortex as measured by radioactive microspheres. The fractional outer/inner cortical blood flow changed from 79:21 before histamine to 74:26 during its infusion (P less than .001). Histamine did not alter creatinine clearance (Ccr), urine volume (V), sodium excretion (UNaV) or the fractional excretion of sodium (FENa) or water (FEH20) under these conditions. When renal blood flow was held constant during the infusion of histamine, PP decreased from 126/106 +/- 2 to 100/81 +/- 2 mm Hg (P less than .001). This resulted in a reduction of absolute outer cortical (outer/inner) changed from 77:23 before histamine to 72:28 during its infusion (P less than .001). In contrast to the effects of histamine at constant PP, CCr, V, UNaV, FENa, and FEH20 were decreased when histamine infusion reduced the PP. Administration of the H1 receptor antagonist, diphenhydramine, blocked the hemodynamic effects of histamine whereas the administration of an H2 receptor antagonist, metiamide, did not alter the histamine response. Similar vasodilatory responses to histamine were observed in isolated blood perfused dog and cat kidneys. In contrast, vasoconstrictor responses to histamine occurred in isolated dog and cat kidneys perfused with Krebs' solution and in isolated rabbit kidneys whether perfused with blood or Krebs' solution.

Animals↗
PubMed1999

Effects of intrapancreatic neuronal activation on cholecystokinin-induced exocrine secretion of isolated perfused rat pancreas.

The role of intrapancreatic neurons in the action of cholecystokinin (CCK) on pancreatic exocrine secretion of the totally isolated, perfused rat pancreas was investigated. Intrapancreatic neurons were activated by applying electrical field stimulation (EFS) to the isolated pancreas for 45 min. When applying EFS, spontaneous pancreatic secretions of fluid and amylase increased until the second 15-min period of EFS and then decreased during the third 15-min period. Atropine (2 microM) notably reduced the EFS-evoked pancreatic secretions of fluid and amylase. The CCK-induced (10 pM) pancreatic secretions of fluid and amylase elevated further in the first 15-min period of EFS and then gradually resumed to the levels observed during application of CCK alone in the third 15-min period of EFS. However, the CCK-induced pancreatic secretions remained elevated even in the third 15-min period of EFS when an action of endogenous somatostatin was inhibited by cyclo-(7-aminoheptanonyl-Phe-d-Trp-Lys-Thr[BZL]) (10 nM) or pertussis toxin (200 ng/ml). EFS further elevated spontaneous exocrine secretion by the cysteamine-treated (300 mg/kg) pancreas, but this was markedly reduced, to normal levels, by infusing somatostatin (100 pM). EFS increased the numbers of immunoreactive somatostatin cells in the Langerhans' islets. The results indicate that intrapancreatic neuronal activation influences CCK-induced pancreatic secretions in a dual-phase pattern in the rat: an increase during the early phase and a decrease during the late phase. Endogenous somatostatin released from the islets appears to inhibit the enhancing effect of neuronal activation on CCK-induced pancreatic secretion. Of the intrapancreatic neurons, the cholinergic ones appear to predominate in EFS's effects on CCK-induced pancreatic secretion.

Amylases↗
PubMed1998

Hepatic disposition and toxicity of cationized goat immunoglobulin G and fab fragments in isolated perfused rat liver.

Colchicine-specific goat IgG and Fab fragments were cationized by covalent coupling of hexamethylenediamine. The immunoreactivity of antibodies was not changed following cationization. The interaction of 125I-radiolabeled native (nIgG and nFab) and cationized immunoglobulin G (cIgG) and Fab fragments (cFab) with liver was investigated using isolated perfused rat liver (IPRL) and isolated rat hepatic parenchymal cells (PCs) and nonparenchymal cells (NPCs) in suspension. 125I-cIgG or 125I-cFab were more rapidly cleared from the perfusate than the corresponding native proteins. Both cIgG and cFab declined biexponentially over time in the perfusate. In contrast, the native IgG and Fab decreased monoexponentially. The half-lives of the initial and terminal phases were 5.2 +/- 1.6 min and 355.1 +/- 17.2 min for cIgG and 14.7 +/- 3.4 min and 552.4 +/- 23.7 min for cFab. The terminal half-lives of nIgG (467.4 +/- 11.6 min) and nFab (880.1 +/- 39.6 min) were longer than those of cationized molecules. The biliary protein extraction ratio of cationized IgG and Fab was greater than that of native IgG and Fab: 0.13% (cIgG), 0.02% (nIgG), 0.23% (cFab), and 0.17% (nFab). The uptake of cIgG and cFab by both PCs and NPCs was dose-dependent and was about 6-fold and 8-fold higher than that of their native counterparts, respectively. Throughout the experiment, liver viability was determined, and no toxicity was observed according to physiological analysis (bile flow rate, portal vein pressure, and pH) and biochemical analysis (glucose and hepatic enzymes: alanine transaminase, aspartate transaminase, lactate dehydrogenase) in perfusate.

Animals↗
PubMed1999

A collaborative approach to isolated limb perfusion.

Isolated limb perfusion is used to treat unresectable sarcoma, melanoma, and other select tumors. It is performed in the OR and requires collaboration by surgeons, perioperative nurses, anesthesia care providers, pharmacists, perfusion technologists, and nuclear medicine personnel. The procedure involves complete isolation of the vascular supply to a limb before an infusion of high dose chemotherapeutic medications.

Antineoplastic Agents, Alkylating↗
PubMed1984

A microelectrode for continuous monitoring of glucose concentration in isolated perfused tubule segments.

The design and the application of a micro-enzyme-electrode for continuous monitoring of glucose concentration in the isolated tubule preparation is described. The principle of the electrode is the amperometric detection of hydrogen peroxide, which is a product of the oxidation of D-glucose by glucose oxidase immobilized at the tip of a micro-electrode. The resulting current causes a voltage deflection across a resistor in series with the electrode that is correlated directly with the glucose concentration. The electrode response to glucose is almost linear over the concentration range from 0 to 12 mmol/l with a slightly diminished slope in the higher range. Other sugars (12 mmol/l raffinose, galactose, fructose, sucrose, mannitol), pH (from 6.5 to 8.0) and pCO2 (from 1 to 10 kPa) do not influence the reading. A reduction of pO2 in the test solution to 1 kPa blunts the reading. Raising the temperature from 20 degrees C to 40 degrees C leads to a pronounced increase of the voltage deflection at a given glucose concentration. Interference is observed with strongly reducing agents such as L-cysteine, ascorbic acid and uric acid. At defined conditions the electrode is well suited to measure continuously glucose concentration in the luminal fluid at the collection site of the isolated perfused tubule of the kidney. Experiments are presented which illustrate the performance of the glucose electrode in this isolated tubule set-up. Peritubular reduction of potassium concentration or the application of ouabain diminish glucose reabsorption.

Animals↗
PubMed1992

Effects of Ca2+ agonists on cytosolic Ca2+ in isolated hepatocytes and on bile secretion in the isolated perfused rat liver.

The effects of increases in cytosolic Ca2+ on hepatocyte bile secretion are unknown. A number of agents that alter levels of cytosolic Ca2+ in the hepatocyte also produce hepatic vasoconstriction and activate protein kinase C, which complicates interpretations of their effects on bile secretion. To better understand the role of cytosolic Ca2+ in bile secretion, we examined the effect of the Ca2+ ionophore A23187 (0.1 mumol/L), the Ca2+ agonist vasopressin (10 nmol/L) and the Ca(2+)-mobilizing agent, 2,5-di(tert-butyl)-1,4-benzohydroquinone (25 mumol/L) on cytosolic Ca2+ in isolated hepatocytes and on bile flow in the isolated perfused rat liver, using vasodilators and inhibitors of protein kinase C and Ca2+ influx. Single-pass perfused livers were used, and cytosolic Ca2+ was measured by luminescent photometry in isolated hepatocytes loaded with the Ca(2+)-sensitive photoprotein aequorin. After A23187 perfusion, a sustained 74% +/- 10% (mean +/- S.D.) decrease in bile flow and a sustained 271% +/- 50% increase in perfusion pressure was observed. Simultaneous pretreatment with the vasodilator papaverine (25 mumol/L) and the protein kinase C inhibitor H-7 (50 mumol/L) abolished the pressure increase but not the decrease in bile flow, whereas pretreatment with Ni2+ (25 mumol/L) to block the influx of extracellular Ca2+ markedly reduced both the pressure increase and the decrease in bile flow. Vasopressin produced a transient (mean = 6 min) 75% +/- 4% decrease in bile flow and a sustained 7% +/- 4% increase in perfusion pressure. Pretreatment with H-7 alone corrected the vasopressin-induced pressure increase but also failed to eliminate the decrease in bile flow, whereas pretreatment with Ni2+ decreased the magnitude of the decrease by two-thirds without affecting the increase in perfusion pressure, 2,5'-di(tert-butyl)-1,4-benzohydroquinone produced a transient 65% +/- 20% decrease in bile flow and a transient 56% +/- 15% increase in perfusion pressure. In isolated hepatocytes, bromo-A23187, the nonfluorescent form of the ionophore, produced a sustained 56% +/- 32% increase in the cytosolic Ca2+ signal, whereas vasopressin resulted in a transient 241% +/- 75% increase and 2,5-di(tert-butyl)-1,4-benzohydroquinone resulted in a sustained 149% +/- 66% increase. The ionophore-induced increase in Ca2+ was abolished completely by pretreatment of the hepatocytes with Ni2+, whereas the vasopressin-induced increase was reduced by 38%.(ABSTRACT TRUNCATED AT 400 WORDS)

Aequorin↗
PubMed1976

The insulinotropic action of gastric inhibitory polypeptide in the perfused isolated rat pancreas.

Gastric inhibitory polypeptide (GIP) produced a dose-related increase in immunoreactive insulin (IRI) from the perfused isolated rat pancreas. The doses employed were within physiological limits. This effect was glucose-concentration-dependent in that there existed a threshold concentration of glucose above which GIP exerted the insulinotropic action, and that, at a fixed concentration of GIP, increased glucose concentrations stimulated IRI release in more than an additive manner. A biologically active fragment of the GIP molecule was isolated and purified. All criteria have been satisfied that GIP is an insulinotropic hormone.

Animals↗
PubMed1998

Effect of multidrug resistance modulators on the hepatobiliary disposition of doxorubicin in the isolated perfused rat liver.

P-Glycoprotein (P-gp)-mediated multidrug resistance (MDR) in cancer cells may be modulated by competitive inhibitors of P-gp. In the liver, P-gp is localized on the canalicular membrane of hepatocytes. Quinidine and GF120918 inhibit the transport of P-gp substrates, including doxorubicin. Competitive inhibition of P-gp transport may alter biliary excretion of substrates. This study was designed to examine the effects of MDR modulators on the hepatobiliary disposition of doxorubicin and to elucidate the site(s) of drug-modulator interaction using pharmacokinetic modeling techniques. Livers from male Sprague Dawley rats were isolated and perfused for 2 h at 37 degrees C with recirculating male rat blood. MDR modulator (16.8-480 microg of GF120918 or 0.3-3.0 mg of quinidine) or vehicle (buffer or DMSO, respectively) was administered as a bolus to the perfusate reservoir 5 min prior to the addition of doxorubicin (464 microg). Perfusate and bile were collected during the perfusion, the liver was homogenized after the perfusion, and samples were analyzed by high-pressure liquid chromatography for doxorubicin and the major metabolite doxorubicinol. In the presence of GF120918, the biliary excretion of doxorubicin and doxorubicinol was decreased significantly without alterations in doxorubicin perfusate concentrations or doxorubicin and doxorubicinol liver concentrations. In the presence of quinidine, the biliary excretion of doxorubicin was reduced significantly; however, doxorubicinol recovery in bile was not altered. The perfusate and liver concentrations of doxorubicin were not altered by quinidine; doxorubicinol liver concentrations were increased. A series of pharmacokinetic models were evaluated incorporating perfusate, liver, and bile compartments to describe the disposition of doxorubicin and doxorubicinol in the isolated perfused rat liver. The model that best described these data, based on goodness-of-fit criteria, included first-order rate constants for all disposition processes. On the basis of this model, the rate-limiting process for doxorubicin and doxorubicinol elimination was biliary excretion. In the presence of GF120918, rate constants associated with doxorubicin and doxorubicinol canalicular egress were decreased, and other doxorubicinol disposition pathways were increased slightly. Quinidine was associated with a decrease in doxorubicin canalicular egress, doxorubicinol formation, and other doxorubicinol pathways. Pharmacokinetic modeling of the data supported the hypothesis that decreased biliary excretion of doxorubicin in the isolated perfused rat liver, as determined by mass-balance analysis, was due to interactions at the canalicular membrane. The present study further supports the utility of pharmacokinetic modeling in identifying sites of drug interactions within the hepatobiliary system. This approach may be particularly useful in predicting the effects of perturbations in hepatic translocation processes on the hepatobiliary disposition of drugs and derived metabolites.

Acridines↗
PubMed1993

Urinary epidermal growth factor is excreted from the rat isolated perfused kidney in the absence of plasma.

Large amounts of epidermal growth factor (EGF) are excreted in urine and the majority of this urinary EGF appears to be of renal origin. EGF is synthesized in the kidneys as a membrane-bound 160 kDa precursor, in the thick ascending limb of Henle and in the early part of the distal convoluted tubule. Very little is known about how EGF is released from cell membranes into urine but proteolytic cleavage of the membrane-bound EGF precursor seems likely. The purpose of this study was to examine whether plasma constituents are necessary for urinary excretion of EGF. In the rat isolated kidney perfused at a pressure of 90 mmHg with a modified Krebs-Henseleit buffer containing oncotic agents, the quantity of EGF excreted into the ureteral effluent was 67% of the amount excreted by the rat kidney in vivo. The EGF excreted by the isolated kidney behaved like urinary EGF upon gel filtration. Administration of the proteinase inhibitor aprotinin reduced urinary EGF excretion from the rat isolated perfused kidney by approximately 50%. In conclusion, the rat isolated perfused kidney excreted significant amounts of urinary EGF without having access to plasma, and EGF excretion was reduced by aprotinin. This is further evidence suggesting an intrarenal source of urinary EGF and suggests that the EGF precursor in the rat kidney is processed by enzyme(s) of renal origin.

Animals↗
PubMed1989

Functional morbidity after regional isolated perfusion of the limb for melanoma.

A series of 57 patients still in follow-up after regional isolated perfusion (RIP) of Stage I-II high-risk melanoma is described. Functional morbidity of the perfused limb was investigated. Median interval after RIP was 5 years. With no regard to recurrent disease subjectively only one patient had severe complaints of the perfused limb. Objective investigation showed no edema or atrophy in 80% of the upper limbs and in 64% of the lower limbs. Concerning the mobility of the joints in the upper limb we found in four cases a disturbed function in several movements. More restriction were observed in the lower leg. Especially the ankle showed severe functional restrictions in more than 25%.

Ankle Joint↗
PubMed1990

The role of iron and glutathione in t-butyl hydroperoxide-induced damage towards isolated perfused rat livers.

The hepatotoxic and lipid peroxidative potentials of t-butyl hydroperoxide (t-BuOOH) towards isolated perfused rat livers were investigated at doses of 1 and 3 mmol l-1. t-BuOOH led to a concentration-dependent release of cytosolic (glutamate-pyruvate transaminase and lactate dehydrogenase) and mitochondrial (glutamate dehydrogenase) enzymes, an accumulation of calcium in the liver, a marked depletion of hepatic glutathione and an enhanced release of it into the perfusate, as well as an enhanced formation and release of malondialdehyde (MDA) by the liver. These effects were blocked in the presence of the potent iron chelator deferrioxamine, and enhanced in livers from iron-overloaded as well as in livers from glutathione-depleted rats. Our results indicate that the hepatotoxic and pro-oxidant actions of organic hydroperoxides depend upon the presence of ionized iron as a catalyst of radical-forming breakdown reactions, and are potentiated by impairment of glutathione-dependent detoxification reactions.

Alanine Transaminase↗