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Biomedical subjects

I Posner

Publications and source records attributed to I Posner.

At least 37 records · Page 2Linked to original sources
PubMed1983

The comparative kinetics of soluble and heparin-Sepharose-immobilized bovine lipoprotein lipase.

While lipoprotein lipase (LPL) acts in vivo as an immobilized enzyme, its kinetics are commonly studied with soluble LPL (S-LPL). Hence kinetic parameters of S-LPL and heparin-Sepharose-immobilized LPL (B-LPL) were compared. A modified purification procedure for bovine milk, LPL gave a 56% yield of S-LPL, purified 7250-fold, and a specific activity of 27,000 mumol fatty acid/mg LPL/h when assayed with triolein (TG) emulsions in the presence of serum. The purified LPL also showed low but detectable esterase activity with p-nitrophenylacetate and p-nitrophenylbutyrate as substrates. Apolipoprotein C-II (C-II) had no effect on the esterase activity of LPL. Dixon plots of experiments with S-LPL indicated that heparin is a competitive inhibitor against both C-II and TG, and that the binding of either C-II or heparin to the enzyme is a mutually exclusive event. Similarly, the binding of TG and heparin to the enzyme is mutually exclusive. From the Dixon plots, the dissociation constant Ki for the LPL:heparin binary complex was determined to be 5.0 X 10(-8) M. In contrast to the heparin inhibitory effect on LPL activity against triolein, heparin had no effect on the esterase activity of LPL against p-nitrophenylacetate or p-nitrophenylbutyrate. Comparative studies with B-LPL and S-LPL, using triolein as substrate and apolipoprotein C-II or serum as activator, indicated that S-LPL has a higher apparent Km and lower apparent Vmax than B-LPL. It is concluded that most of the LPL bound to heparin-Sepharose is probably inaccessible to substrate, hence a low Vmax. However, Km (C-II) and Km (TG) were higher for B-LPL due to the competitive inhibitory effect of heparin on LPL. Consistent with these kinetic analyses and with the use of human very low density lipoproteins (VLDL) as substrate, S-LPL, even in the presence of heparin, was found to have an apparent rate of lipolysis of VLDL approximately ninefold greater than B-LPL.

Animals↗
PubMed1983

Kinetics of bovine milk lipoprotein lipase and the mechanism of enzyme activation by apolipoprotein C-II.

The kinetics of bovine milk lipoprotein lipase (LPL) were studied in order to determine the reaction mechanism of this enzyme. Reaction velocities were determined at varying concentrations of emulsified trioleoylglycerol (TG) and different fixed concentrations of apolipoprotein C-II (C-II) or at varying C-II concentrations and different fixed concentrations of TG. Neither the apparent Km(TG) nor the apparent Km(C-II) was affected by varying the concentrations of C-II or TG, respectively. However, C-II increased the apparent Vmax for the enzyme about 20-fold. The following kinetic parameters were calculated from Lineweaver-Burk plots: Km(C-II) = 2.5 X 10(-8) M and Km (TG) = 2.5 X 10(-3) M. The dissociation constant (KS) of the enzyme-TG binary complex was determined from Scatchard plots to be 7.6 X 10(-8) M. Heparin was found to be a competitive dead-end inhibitor against both TG and C-II. Tricapryloylglycerol represented a competitive inhibitor against TG but a noncompetitive inhibitor against C-II. C-II was shown to interact with dansylated bovine milk LPL, increasing its fluorescent emission by inducing a conformational change in the enzyme. Based on these studies, it was concluded that the LPL-catalyzed reaction follows a random, bireactant, rapid-equilibrium mechanism and the role of C-II in the activation process involves an increase in the catalytic rate constant (Kp) resulting from conformational changes of LPL induced by C-II.

Animals↗
PubMed1981

Arousal of sexual and aggressive contact by exposure to stressors in albino rats.

Since certain forms of aggressive and sexual activity are associated with elevated adrenal steroid activity, the hypothesis explored here was whether subjection to a stressful environment which is known to elevate adrenal output would arouse both sexual and aggressive behavior. Accordingly, 24 male Sprague-Dawley rats were subjected to either physical restraint and heat or a nonstress control environment for 13 days. Following this treatment Ss were tested for sexual and aggressive behavior. As predicted, the stressed Ss showed increased levels of ano-genital sniffing of an estrus female, as well as increased intermale aggressiveness.

Aggression↗
PubMed1978

Effects of combining pilocarpine, d-amphetamine, and either a free feeding schedule or cyclic food deprivation on mouse killing by rats.

The combination of a drug which suppresses mouse killing by rats (d-amphetamine) , a drug which activates mouse killing (pilocarpine), and either ad-lib food or a 24-hour cyclic food deprivation schedule were examined for their effects on the mouse-killing response by rats (N = 53). Results showed that the presence of d-amphetamine prevented the activating effects of pilocarpine in rats with a fairly high killing propensity regardless of whether they were on the ad-lib food or the deprivation schedule. The study suggests that a drug which affects both eating behavior and mouse killing is more effective in determining behavioral outcomes than a drug which affects only mouse killing.

Aggression↗