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PubMedDate not supplied

Metabolism of benzo[a]pyrene by the isolated perfused rabbit lung.

The metabolism of benzo[a]pyrene (BP) was studied in the isolated perfused rabbit lung and in rabbit pulmonary microsomes. Pretreatment of rabbits with 3-methylcholanthrene did not increase the metabolism of BP by microsomal preparations, and the pretreatment did not induce cytochrome P-448 in pulmonary microsomes. In the isolated perfused lung, BP was metabolized at a rate of about 6 nmol/min/g of lung. The intermediate arene oxides formed from BP in the isolated perfused lung were metabolized nonoxidatively by epoxide hydrase and glutathione S-transferases. The rates of the latter reactions were at least an order of magnitude less than the overall rate of metabolism. Pretreatment of the animals with 3-methylcholanthrene increased only the apparent rate of the epoxide hydrase reaction. In the isolated perfused lung, BP and some of its less polar metabolites (i.e., quinones and phenolic derivatives) were preferentially partitioned into lung tissue, precluding accurate measurement of metabolic rates by analysis of the perfusion medium alone. Covalent binding of BP-derived radioactivity to lung tissue occurred, but relatively high variability in this parameter in lungs from 3-methylcholanthrene-pretreated animals did not allow measurement of a significant difference from control lungs.

Animals↗
PubMed1997

Nephrotoxic effects of bacterial ribonucleases in the isolated perfused rat kidney.

Alterations of the renal function in the isolated perfused rat kidney system after application of two bacterial RNases, Bacillus intermedius RNase (binase) and ribonuclease produced by Bacillus amyloliquefaciens (barnase), were investigated with two different treatment regimens in comparison with catalytically inactive derivates of the enzymes, photooxidated at the active site His101 binase and inactive mutant His102Gln barnase. For the in vitro approach the test enzymes were dissolved in the perfusion media and applied to the kidney after removal from the animal. Alternatively, the test ribonucleases were administered to rats in vivo and the renal effects were assessed in the isolated perfused rat kidney 1 and 6 h after treatment. In the in vitro regimen both active enzymes induced time- and concentration-dependent nephrotoxicity reflected in enhancement of urinary protein excretion, decline of glucose reabsorption, increase of gamma-glutamyltranspeptidase and alkaline phosphatase activities in urine. In vivo administration of active binase induced functional impairment of the isolated perfused organ in a similar way. None of the inactive RNases in both regimens and at all concentrations tested altered any renal parameter. The results suggest that RNA degradation may be involved in the nephrotoxic effects of bacillar RNases.

Alkaline Phosphatase↗
PubMed1989

Study of hepatotoxicity in isolated perfused liver versus cultures of rat hepatocytes.

Isolated perfused liver and cultures of rat hepatocytes were assessed for the quantitative evaluation of hepatotoxicity. Release of de novo biosynthesized plasma proteins and acid hydrolases into perfusion or culture media was taken as an indication of the integrity of hepatocytes in both systems. The activities of six acid hydrolases, alpha-L-fucosidase, alpha-D-galactosidase, beta-D-galactosidase, beta-D-N-acetylgalactosaminidase, beta-D-N-acetylglucosaminidase, and cathepsin D, were assayed in collagenase-segregated hepatocytes and in monolayer cultures of rat liver cells obtained via collagenase perfusion of rat liver. In situ, liver perfusion with collagenase led to a loss of 45 +/- 5% of the total acid hydrolase activity in the mitochondrial-lysosomal pellet of the liver cells with concomitant increase of these enzymes in the cytosol. In monolayer cultures over a period of 30 h, increased activity of cathepsin D, beta-D-galactosidase, and beta-D-N-acetylglucosaminidase in the mitochondrial-lysosomal pellet and the cytosol fraction was evident with concurrent biosynthesis of plasma proteins. The use of radioactive tracing techniques with the isolated perfused liver revealed that the rate of catabolism of intracellular protein was approximately 5 times that of plasma protein synthesis. Both methods described here are suitable for the study of the effects of toxins on the function of hepatocytes.

Animals↗
PubMed2002

Agonist-induced vasoactive responses in isolated perfused porcine dental pulpal arterioles.

A novel isolated perfused pulpal arteriole preparation and microperfusion system was used to evaluate the direct vasoactive responses of pulpal arterioles to selected agonists. Short lengths of porcine pulpal arterioles (101.7+/-2.2 microm o.d., n=105) were dissected out and placed in an environment-controlled bath on the stage of an inverted microscope. Both ends of the vessel were cannulated and perfused at a controlled rate through the lumen. The diameter of the vessel was measured online. Following equilibration, the vessel was challenged with various agonists: adrenaline (epinephrine), noradrenaline (norepinephrine), phenylephrine, dopamine, isoproterenol, 5-hydroxytryptamine, histamine and adenosine. The endothelium-dependent vasodilator acetylcholine was used to evaluate endothelial cell function. Adrenaline, noradrenaline, phenylephrine, 5-hydroxytryptamine and dopamine caused dose-dependent contractions (adrenaline=noradrenaline>phenylephrine>dopamine>5-hydroxytryptamine). Isoproterenol and histamine provoked a dose-dependent dilation. Adenosine produced pronounced vasodilatation in vessels precontracted with 10(-8)M endothelin-1. Functional adrenergic, histamine, 5-hydroxytryptamine and adenosine receptors are, therefore, present in porcine pulpal arterioles. The isolated perfused pulpal arteriole preparation may prove valuable in understanding local control mechanisms of pulpal microcirculation.

Adenosine↗
PubMed1984

Release of active and inactive kallikrein from the isolated perfused rat kidney.

The release of kallikrein into the perfusate and urine of the isolated perfused rat kidney was studied. Comparison between enzymic and immunological assays for kallikrein demonstrated the presence of an enzymically inactive form of kallikrein. Of kallikrein found in normal rat urine 77 +/- 4% is active and 23% is in an inactive form. In the isolated perfused rat kidney a similar proportion of active kallikrein (84%) was excreted into the urine but very little enzymically active kallikrein (2%) could be detected in the perfusate. However, significant amounts of enzymically inactive but immunologically reactive kallikrein could be found in the kidney perfusate. The rate of release of kallikrein into the perfusate was approximately one-fifth of the rate of release into the urine. Renin showed a similar pattern of release into the perfusate and urine but the lysosomal enzyme marker acid phosphatase was not detectable. These results show that kallikrein is secreted from the kidney into the circulation as well as being excreted in the urine. However, in urine the enzyme is predominantly in an enzymically active form whereas it is secreted into the circulation in an inactive form.

Acid Phosphatase↗
PubMed1996

Arrhythmogenic action of endothelin peptides in isolated perfused whole hearts from guinea pigs and rats.

The arrhythmogenic actions of endothelin peptides were studied in isolated perfused hearts from guinea pigs and rats. Digoxin-induced ectopic ventricular complexes were partially antagonized by phosphoramidon, an endothelin-converting enzyme inhibitor. On the contrary, these rhythm disturbances were potentiated by big endothelin-1 in isolated perfused whole hearts from guinea pigs. Endothelin-1, when infused through the coronary circulation at a concentration of 10(-10) mol/l, produced an increase in coronary perfusion pressure without altering the heart rate and contractility in the isolated perfused hearts of rats. However, ventricular ectopic complexes occurred when the rise in coronary perfusion pressure reached the peak value. BQ 485, an endothelin-A receptor antagonist, at a concentration of 10(-6) mol/l, completely blocked the vasoconstrictor and arrhythmogenic effects of endothelin-1. In BQ 485-pretreated rat hearts, endothelin-1 produced a fall in coronary perfusion pressure and a slight positive inotropic response which could be blocked by NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor. BQ 485 at the same concentration also caused a significant reduction in the duration but not the onset of ventricular ectopic complexes in the guinea pig isolated perfused heart induced by digoxin. These results were taken as evidence of the arrhythmogenic action of endothelin peptides and their possible participation in the ventricular dysrhythmia induced by digoxin.

Animals↗
PubMed1990

Effects of perfusion pressure and renal flow upon albumin excretion in isolated perfused kidneys.

To explore the effects of renal hemodynamics upon urinary albumin excretion, sequential changes in perfusion pressure and/or flow were performed in isolated perfused rat kidneys. Elevation of perfusion pressure from 90 to 130 mm Hg increased renal flow from 48.9 +/- 1.1 to 54.3 +/- 1.4 ml/min and glomerular filtration rate (GFR) from 0.37 +/- 0.03 to 0.81 +/- 0.06 ml/min (p less than 0.001). Despite more than a doubling in GFR, albumin excretion remained unchanged (from 252 +/- 53 to 167 +/- 36 micrograms/min, p not significant), resulting in a decreased fractional clearance of albumin (theta) from 0.009 +/- 0.002 to 0.004 +/- 0.005 ml/min (p less than 0.01). To dissociate the effects of flow from those of pressure, angiotensin II was infused to decrease renal flow from 49.9 +/- 0.6 to 38.7 +/- 0.6 ml/min (p less than 0.001), while keeping perfusion pressure constant at 96 +/- 1 mm Hg. Although GFR was essentially unchanged (from 0.59 +/- 0.02 to 0.65 +/- 0.05 ml/min, p not significant), albumin excretion increased from 68 +/- 8 to 151 +/- 21 micrograms/min (p less than 0.001) and theta rose from 0.002 +/- 0.000 to 0.005 +/- 0.001 (p less than 0.02). Whole kidney hemodynamics acutely affect renal excretion of albumin in isolated kidneys.

Albuminuria↗
PubMed1980

Pharmacological studies of neurotensin, several fragments and analogous in the isolated perfused rat heart.

Neurotensin (NT) induced a dose-dependent increase of the coronary perfusion pressure (CPP) in the isolated perfused rat heart. This effect was not modified by pretreating the organ with methysergide (8.5 x 10(-6) M), atropine (3.4 x 10(-6) M), a mixture of phentolamine (3.1 x 10(-6) M) and practolol (1.5 x 10(-5) M), 8-leucine-angiomine (2.9 x 10(-5) M) thus suggesting the existence of specific NT receptors in the coronary vessels of rat. The structure-activity studies performed using several NT fragments and analogues in the isolated perfused rat heart led us to the following conclusions: (1) the minimum structure required for the full expression of the biological activity of NT is H-Arg9-Pro10-Tyr11-Ile12-Leu13-OH; (2) the amino acid Tyr in position 11 appears to play a key role in the process of NT receptor activation. The replacement of Tyr11 with Tyr(Me) gave a compound which inhibits selectively the increase in coronary perfusion pressure induced by NT, but still exhibits some NT-like activity, specially when used in concentrations higher than 10(-6) M. [Tyr(Me)11]NT did not antagonize the stimulant effects of NT in rat stomach strips and guinea pig atria, thus suggesting that the receptors mediating the constrictor effect of NT in coronary vessels of the rat are pharmacologically different from those subserving the stimulant effect of NT in rat stomach strip and guinea pig atria.

Animals↗
PubMed1977

Isolated perfused lung--substrate utilization.

Lung metabolism has been extremely difficult to determine in vivo primarily because the lung is overwhelmed by a great blood flow that generally makes the Fick principle inadequate. Largely for reasons such as this, investigators have had to rely on in vitro preparations. The isolated perfused lung has the apparent advantage of being similar to the lung in vivo when compared with other preparations. For instance, there is evidence that the capillary bed of the lung may alter substrates and influence their subsequent metabolism. Substrates have contact with the capillary endothelium in isolated perfused lungs but not to tissue slices, homogenates, or isolated cells. Our studies indicate that precursors of saturated phosphatidylcholine may include lipids, which are hydrolyzed in the capillary of the isolated perfused lung and thus become substrates such as free fatty acids, etc. However, tissue slices do not use the esterified lipids to the same extent, presumably because in this preparation the enzymes in the capillary endothelium do not have contact with the esterified lipids. Substrate utilization of the isolated perfused lung may be considerably altered by inflation of the lung or by pulmonary edema. Although glucose utilization and palmitate oxidation by the isolated perfused lung and by tissue slices of the rat lung are very similar, if the isolated perfused lung develops pulmonary edema, glucose utilization increases by nearly 100%. This phenomenon is apparently not due solely to fluid in the airspaces because in control studies with fluid added into the airways the glucose utilization did not increase to the degree observed with edematous lungs. Lung distention is associated with increased glucose consumption but marked distention is also associated with pulmonary edema. The effect of lung distension may be a direct effect or it may be secondary to the pulmonary edema.

Animals↗
PubMed1996

Renovascular responses to high and low perfusate calcium steady-state experiments in the isolated perfused rat kidney with baseline vascular tone.

Acute hypercalcemia is commonly observed in surgical patients after calcium infusion while acute hypocalcemia is common during rapid citrated blood transfusion. Although high and low ionized calcium ([Ca2+]) within the clinical range produce an increase or decrease in cardiac performance and systemic vessel resistance, respectively, their effects on renal vessels have not been quantified. A possible renal vasoconstriction that might occur with high [Ca2+] is of clinical interest because it is a factor which may contribute to impaired renal circulation and decreased function. In this study we examined the renovascular responses to [Ca2+], which was varied within the clinical range under hemodynamically controlled conditions. We instituted high and low [Ca2+] in the per fusate, which consisted of Krebs-Henseleit buffer containing albumin, 60-65 g/liter. Stable high (n = 10) or low (n = 7) [Ca2+] (1.93 +/- 0.02 and 0.59 +/- 0.01 mM, respectively) was instituted for 10 min and preceded and followed by normal [Ca2+] of the same duration. In a separate protocol (n = 8) verapamil (10(-5) M) was added to the perfusate 10 min before high [Ca2+] was tested. We measured changes in renal flow at a constant perfusion pressure of 110 mm Hg and also characterized the renal vessels over a range of pressures by pressure vs flow plots. High [Ca2+] was associated with a small decrease in flow (from 28.8 +/- 2.4 to 26.9 +/- 2.6 ml/min/g, P < 0.02), indicating a small vasopressor effect. This effect was also shown by a leftward shift in the pressure vs flow plots. These changes were prevented by verapamil. GFR decreased (from 0.35 +/- 0.04 to 0.28 +/- 0.06 ml/min/ g, P < 0.01) without a significant change in sodium excretion or fractional sodium excretion. Low [Ca2+] was associated with increased renal flow (from 30.8 +/- 2.1 to 35.2 +/- 2.7 ml/min/g, P < 0.02), indicating a vasodilator effect. This effect was also shown by a rightward displacement of the pressure vs flow plots. GFR increased from 0.51 +/- 0.03 to 0.56 +/- 0.04 ml/min/ g, P < 0.01, as did sodium excretion (from 2.32 +/- 0.22 to 3.87 +/- 0.49 microEq/min, P < 0.01) and fractional sodium excretion (from 2.33 +/- 0.26 to 3.61 +/- 0.49%, P < 0.01). We conclude, first, that in the isolated perfused rat kidney, high [Ca2+] is a weak vasopressor while low [Ca2+] has vasodilator action. Second, high [Ca2+] effects are abolished by verapamil pretreatment. These findings illuminate mechanisms of high [Ca2+] effects on renovascular tone.

Animals↗
PubMed2006

Isolated perfusion of a tubed superficial epigastric flap in a rodent model.

BACKGROUND: Isolated perfusion models can yield important data regarding metabolism of the skin. An effective model must remain stable during perfusion but respond appropriately to metabolic and vascular stimuli. We describe the design and characterization of a tubed superficial epigastric isolated perfusion flap. MATERIALS AND METHODS: Tubed superficial epigastric flaps were created in 20 male Sprague Dawley rats. Forty-eight hours later the femoral vessels were cannulated and the flaps were perfused using a Krebs-Heinseleit buffer containing albumin for a period of 2 h. In five of the flaps norepinephrine and acetylcholine were added sequentially to the perfusate to determine vascular reactivity. In a further four flaps insulin (20 U/liter) and iodoacetate (5 mM) were added to the perfusate to confirm that the flap was metabolically active and reactive. Venous outflow was collected at regular intervals and analyzed for electrolytes, lactate, and glucose content. Vascularity and skin perfusion were characterized using barium microangiography and methylene blue dye injection. RESULTS: This flap model was found to be stable in terms of arterial pressure, electrolyte levels, and lactate production over the perfusion period. Norepinephrine caused a sharp increase in vascular resistance, which was reversed by administration of acetylcholine. Lactate production increased appropriately with the addition of insulin to the perfusate with a rapid decline following addition of the glycolysis inhibitor iodoacetate. There was no leakage of perfusate or significant swelling of the flap during the perfusion. CONCLUSIONS: The tubed superficial epigastric artery flap makes an effective model for isolated perfusion studies of the skin with a wide range of experimental applications.

Acetylcholine↗
PubMed2001

Schisandrin B modulates the ischemia-reperfusion induced changes in non-enzymatic antioxidant levels in isolated-perfused rat hearts.

Isolated Langendorff-perfused rat hearts were subjected to a fixed period of ischemia followed by increasing periods of reperfusion for investigating the changes in the extent of ischemia-reperfusion (IR) injury and tissue levels of non-enzymatic antioxidants. Effects of schisandrin B (Sch B) and (+/-) alpha-lipoic acid (LA) pretreatment were also examined. A 40-min of ischemia (40-I) followed by 20- or 40-min of reperfusion (20-R or 40-R) caused sustainable tissue damage in isolated hearts, as indicated by the increased extent of lactate dehydrogenase (LDH) leakage and impaired contractile force. The myocardial IR injury was associated with a marked decrease in tissue ascorbic acid (V(C)) level. However, myocardial reduced glutathione (GSH) and alpha-tocopherol (V(E)) levels remained relatively unchanged except under a more severe IR condition (40-I, 40-R). Pretreating rats with Sch B or LA at a daily dose of 1.2 mmol/kg for 3 days protected against IR injury in isolated hearts to varying degrees. While only Sch B pretreatment could improve the recovery of contractile force, LA pretreatment produced a better inhibitory effect on LDH leakage. The protection against IR injury was associated with significant increases in myocardial V(E) and V(C) levels in both Sch B and LA pretreated hearts. The ensemble of results suggests that the cardioprotection afforded by Sch B or LA pretreatment may at least in part be attributed to the modulation on the interplay among non-enzymatic antioxidants under oxidative stress induced by IR.

Animals↗
PubMed1992

Effect of vasodilators, including nitric oxide, on the release of cGMP and cAMP in the isolated perfused rat kidney.

In isolated Tyrode-perfused rat kidneys, the release of the cyclic nucleotides cAMP and cGMP was measured in response to several vasodilators, including nitric oxide (NO). During vasoconstrictions induced by methoxamine, a basal release of both cyclic nucleotides was detected in the renal effluent (357 +/- 32 fmol/min for cGMP and 3097 +/- 219 fmol/min for cAMP). Injection of acetylcholine (ACh; 11 nmol), sodium nitroprusside (SNP; 0.8 nmol) and atrial natriuretic factor (ANF; 80 pmol) caused a marked release of cGMP. The cGMP release induced by ACh was not altered by indomethacin (3 microM) but was markedly reduced by the NO synthase inhibitor nitro-L-arginine (L-NNA; 200 microM). Authentic NO (0.16-80 nmol) caused dose-dependent vasodilatations that were accompanied by increases in the overflow of cGMP. The vasodilatations caused by forskolin (6 nmol) and prostacyclin (PGI2; 3-52 nmol) were not accompanied by an overflow of cGMP. The vasodilator responses to 5-hydroxytryptamine (5-HT; 0.25-2 mumol), obtained in presence of the 5-HT2 receptor blocker ritanserin (10 nM) and the 5-HT3 blocker ICS 205930 (10 nM), were markedly reduced by L-NNA; however, they were not accompanied by the renal release of cGMP. Both forskolin and PGI2 induced the release of cAMP from perfused rat kidneys; ACh, 5-HT and 5-carboxamidotryptamine (5-CT) also evoked a significant release of cAMP into the renal effluent. The release of cAMP induced by ACh and 5-HT was reduced by indomethacin and L-NNA. Higher doses of NO released cAMP from the perfused rat kidneys. Our data illustrate that both cAMP and cGMP can be released by vasodilator substances into the venous effluent of isolated perfused rat kidneys. The dilator responses to 5-HT were sensitive to the NO synthase inhibitor L-NNA and were accompanied by the release of cAMP and not by the release of cGMP. Our data suggest that the dilator responses may be due to NO released from endothelial cells, which then activates adenylyl cyclase either directly or indirectly.

Acetylcholine↗
PubMed1990

Low-dose endothelin stimulates release of prostaglandin I2 from isolated perfused hind legs in the rat.

A direct measurement of 6-keto-prostaglandin F1a (6-keto-PGF1a), a stable metabolite of prostaglandin I2, was made in the perfusate from isolated rat hind legs perfused with Krebs-Ringer solution. The rate of release of 6-keto-PGF1a was 5.28 +/- 0.24 ng during the first perfusion period of two min, and it remained stable at least for 40 min. The biological integrity of the preparation was confirmed by inhibition (52%) of 6-keto-PGF1a release by indomethacin (5 X 10(-5) M) in the perfusion medium. Low-dose infusion (5, 10, and 20 pM, for 10 min each) of endothelin (ET) elicited small but significant increment in the release of 6-keto-PGF1a in a dose-dependent fashion; the maximal per cent increase of 6-keto-PGF1a release evoked by ET (20 pM) was approximately +40% over the basal rate. These results taken together with the previous observations of synthesis of ET in the vascular tissue suggest an intriguing relationship between vasoconstrictive ET and vasodilatory prostaglandins in the local control of vascular tone.

6-Ketoprostaglandin F1 alpha↗
PubMed2000

The effect of intraislet somatostatin immunoneutralization on insulin secretion in the isolated perfused rat pancreas.

BACKGROUND: There is evidence of a local inhibitory effect of somatostatin on insulin secretion in the isolated human pancreas, but this has not been shown in a rat model. The possible phasic effect of somatostatin on insulin secretion has not been demonstrated. AIMS: This study was undertaken to determine if somatostatin has a local regulatory effect on phasic insulin secretion within a rat pancreas model. METHODS: The basal and glucose stimulated secretion of insulin was compared with and without immunoneutralization of somatostatin using a somatostatin antibody in an isolated perfused rat pancreas model. High concentration, high affinity monoclonal somatostatin antibody was perfused through isolated rat pancreata. Radioimmunoassay for insulin was performed on the portal effluent. RESULTS: Immunoneutralization of somatostatin during basal insulin secretion produced a rise in insulin secretion of 551 +/- 163% that approached significance. Immunoneutralization during glucose stimulated insulin secretion produced a significant rise in insulin secretion compared to the control group of 2,678 +/- 187% vs. 535 +/- 39% (p < 0.05). The phase I vs. the phase II response in the glucose stimulated pancreas was similar in the presence of control antibody, 867 +/- 351% vs. 900 +/- 398% (p = NS). With somatostatin immunoneutralization, the glucose stimulated pancreas had a significantly higher phase II response than phase I; 3,832 +/- 688% vs. 2,516 +/- 431% (p < 0.05). CONCLUSION: These data indicate that intraislet somatostatin is an inhibitor of insulin secretion in the isolated perfused rat pancreas. This effect occurs primarily in phase II of insulin secretion.

Animals↗
PubMed1986

The relationship between perfusion medium flow rate and steroid secretion in the isolated perfused rat adrenal gland in situ.

Using the in-situ, isolated, perfused rat adrenal preparation, we have investigated the effects of changes in the rate of perfusate flow through the gland, brought about both mechanically and by the use of vasoactive agents, in the absence of known adrenocortical stimulants. Adenosine caused a significant increase in the rate of perfusate flow through the adrenal, with a concomitant rise in corticosterone, but not aldosterone, secretion. Adrenaline, on the other hand, caused a decrease in the rate of perfusate flow through the gland, accompanied by a decrease in the rate of steroid secretion. Furthermore, increases in the rate of delivery of perfusate to the gland, brought about by increasing the peristaltic pump rate, caused a large increase in corticosterone secretion, although aldosterone was unaffected. Neither adenosine nor a mechanically increased rate of perfusate delivery increased steroid secretion by collagenase-dispersed rat adrenocortical cells superfused on a Sephadex column. These results suggest the existence of hitherto unsuspected intraglandular mechanisms for the control of steroid secretion.

Adenosine↗
PubMedDate not supplied

Suppression of lymphocyte activation by a protein released from isolated perfused rat liver.

Isolated rat liver perfusates contain a substance which inhibits 3H-thymidine uptake by phytohemagglutinin-stimulated human peripheral blood lymphocytes in a dose-dependent, noncytotoxic fashion. Suppression is not due to interference of lymphocyte-phytohemagglutinin interaction or dilution of the thymidine pool. Complete inhibition of thymidine uptake is achieved with less than 1.0 microgram of material per ml (which is a potentially achievable concentration in vivo). The release of this material is directly and quantitatively associated with hepatocellular injury as measured by release of glutamic pyruvate transaminase. The material is a highly basic protein with a molecular weight of approximately 65,000 to 80,000 daltons. It is a product of the hepatocyte rather than of nonparenchymal liver cells. Liver-derived materials, such as the presently described molecule, may play a role in in situ regulation of lymphocyte function during immunologically mediated liver disease.

Alanine Transaminase↗
PubMed1978

Transamination of branched-chain keto acids by isolated perfused rat kidney.

Isolated rat kidney perfused without substrate released serine, glycine, and taurine, and substantially smaller amounts of other amino acids. When branched-chain keto acids were added, the corresponding amino acids were released at rates amounting to 15-25% of keto acid disappearance. Perfusion with 2 mM alpha-keto-isovalerate or alpha-keto-beta-methylvalerate caused an increased glucose release amounting to 18-23% of keto acid disappearance. The activity of branched-chain amino acid transferase (BATase) was significantly stimulated by perfusion with the analogue of leucine, but not by perfusion with alpha-ketoglutarate, the analogues of valine or isoleucine, or with leucine itself. These findings document that the kidney converts branched-chain keto acids in part to the corresponding amino acids and suggest that the keto analogue of leucine may be involved in the control of renal BATase activity, thereby indirectly regulating the metabolism of branched-chain amino acids.

Amino Acids↗