Effect Of Hexadecane Research Articles

Synaptobrevin Trans-Membrane Domain forms a Complex that Enhances the Rate of “Stalk” and Pore Formation in PEG-Mediated Vesicle Fusion

Synaptobrevin (SB), a membrane anchored protein in the neuronal cell membrane, complexes with syntaxin (SX) and SNAP-25 to facilitate membrane fusion in neurotransmitter release. SB and SX promote Poly(ethylene glycol) (PEG)-mediated fusion whether or not they are assembled into a SNARE complex (Dennison et al., BJ, 2006, 1661). Viral fusion protein trans-membrane domains (TMDs) enhance the fusion. Thus, we hypothesized that the SB-TMD may also affect fusion kinetics. The kinetics of PEG-mediated fusion of DOPC/DOPE/sphingomyelin/cholesterol/DOPS (32/25/15/20/8) 25 nm vesicles (SUVs) was examined in the presence and absence of SB TMD. Lipid mixing (LM), contents mixing (CM) and leakage (L) time courses were fitted globally to a 3-state sequential model (Weinreb & Lentz, BJ, 2007, 4012), from which we obtained estimates of rate constants for conversion between states as well as probabilities of LM, CM and L for each state. SB TMD enhanced the rates of “stalk” and fusion pore (FP) formation in a cooperative fashion (maximum effect at 3 peptide/vesicle). TMD ordered the bilayer interior in a similarly cooperative fashion. The effects of hexadecane and TMD on fusion kinetics were quite distinct and not mutual. SB TMD increased the probability of both LM and CM in the initial intermediate, suggesting that it promoted formation of transient pores before the final pore state. Transition state thermodynamic changes indicate that the effects on “stalk” and FP formation involved different mechanism, although both showed that in presence of TMD the change in entropy is always greater than enthalpy. Supported by NIH grant GM32707 to BRL.

Effect of the percutaneous administration of hexadecane, 2,4‐dinitrophenol, gas‐oil and fuel‐oil on weight changes in mice

The effects of gas‐oil, fuel‐oil 2,4‐dinitrophenol and hexadecane, the latter either in injection or applied to the skin of mice have been studied in applications scheduled every 12,24 or 48 hours. Studied were effects upon body weight and on the lipid and protein levels of liver and muscle as well as on plasma composition of mice. The effects of all materials tested were very similar, inducing a biphasic effect on body weight: increases with low doses/delayed applications and decreases with high doses/frequent applications. This is tentatively explained as an impairment of the hydric balance as well as effects on thermogenesis through brown adipose tissue oxydative phosphorylation uncoupling elicited by hexadecane. The 3 week treatment with hexadecane resulted in a maintenance of circulating glucose with increases in urea, amino acids and lactate, as well as losses of liver lipids in all groups treated with alkanes or 2,4‐dinitrophenol. The results agree with powerful and lasting effects of hexadecane on...

Alterations of Energy Metabolism Induced by Hexadecane in Mice

Two groups of young male OF-1 mice were fed for 60 days with cafeteria or, as controls, with standard pellet diet respectively. At that time, both groups were daily treated with hexadecane (HDK) on the skin. HDK induced a drastic body weight loss much higher in cafeteria than control mice. White adipose tissue were exhausted after 4 days of treatment in controls but not after 10 days in cafeteria ones. HDK resulted in mobilization of liver glycogen in both groups while muscle glycogen decreased slightly in the end. Hexadecane treatment did not result in massively enhanced nitrogen metabolism, as the actual oxidation of amino acids decreased considerably as indicated by the low levels of plasma urea. The results could be explained by powerful and lasting effects of hexadecane on thermogenesis and metabolic reserve balance. The use of this material for pharmacological manipulation of body weight appeared difficult.

Effect of hexadecane on protein kinase C of pig epidermis.

The application of hexadecane on animals skin induces hyperkeratinization and hyperplasia of the epidermis, however, the initial mechanisms of the epidermal cell proliferation and keratinization by hexadecane stimulation remains unknown. Protein kinase C is reported to be one of the critical enzymes involved in proliferation and differentiation of various cells and tissues. Therefore we investigated the effects of hexadecane on protein kinase C in pig epidermis. Protein kinase C activity of the pig skin increased 10 min after topical application of hexadecane to the back of the pig, normalized at 30 min, and subsequently kept falling for 24 h. In studying hexadecane dropped on floating sliced pig skin in Krebs buffer, similar results were obtained for the short term. Immediately after the hexadecane treatment, protein kinase C activity was not altered as compared with that of the untreated skin. Thus, the alteration of the protein kinase C activity after the hexadecane treatment is not due to the direct effect of hexadecane on the enzyme, but is due to other as yet unknown mechanisms of epidermal cell kinetics in response to hexadecane stimulation. We discuss the mechanisms of protein kinase C activity alteration upon treatment with hexadecane.

Effect of hexadecane on the pharmacokinetics of hexachlorobenzene

Sixty rats were divided into two groups; one group received normal Rat Chow and the other the same feed supplemented with 5% hexadecane. Twenty-four hours later, the rats were injected iv with 1.0 mg/kg [ 14C]hexachlorobenzene (HCB). For 1 month after dosing, the activity of 14C was determined in various tissues and in serum at predetermined intervals. A biexponential decline of radioactivity was observed in serum and tissues of both groups; the decline of 14C in tissues roughly paralleled the decline of radioactivity in serum; exceptions were fat, skin, and the contents of the large intestine, which showed an initial uptake phase. Hexadecane increased the disposition rate constant β in serum, leading to a significantly reduced body burden after 4 weeks of treatment. The more rapid loss of tissue radioactivity was accompanied by increased levels of 14C in intestinal contents of the large intestine. Biliary excretion was unaffected. Data are compatible with describing the kinetics of HCB by a two-compartment open model, where elimination occurs from a part of the peripheral compartment.

Effect of hexadecane on the body burden of hexachlorobenzene in rats

Effect of hexadecane on the body burden of hexachlorobenzene in rats

Enhanced intestinal excretion of hexachlorobenzene in rats by intraluminal injection of hexadecane.

The effect of hexadecane on the intestinal excretion of hexachlorobenzene was studied in female Sprague-Dawley rats dosed twice with 14C-hexachlorobenzene at 50 mg kg-1 per os. Injection of 75 mg n-hexadecane into ligated and unligated segments of the intestine increased concentrations of hexachlorobenzene in intestinal contents by about two- or three-fold in jejunal and ileal segments, and about two-fold in the cecal-colon segment. The jejunum appeared to be the site of greatest excretion of hexachlorobenzene followed by the ileum, the cecum and the colon. This order is opposite to our previous data from animals with an undisturbed intestinal passage. The apparently greater excretion of hexachlorobenzene into the small intestine is probably due to its much larger surface area than that of the large intestine. However, the residency time of luminal contents in the large intestine normally exceeds that in the small intestine by about 20--40-fold, which apparently more than compensates for the difference in relative surface area between small and large intestine. Thus, residency time appears to be a more important factor than surface area in determining the intestinal elimination of hexachlorobenzene. These results with hexachlorobenzene are probably typical of physiological disposition of lipophilic halogenated hydrocarbons generally.

Hexadecane enhances non-biliary, intestinal excretion of stored hexachlorobenzene by rats

[ 14C] Hexachlorobenzene (100 mg/kg) was orally administered to 4 groups of rats. Ten days later the effects of hexadecane (3 × 5 ml/kg by gavage) and/or bile duct ligation on urinary and fecal excretion and tissue levels of hexachlorobenzene, were examined. Hexadecane did not affect urinary excretion of hexachlorobenzene, whereas bile duct ligation tripled it. Each of the 3 treatments ( n-hexadecane, bile duct ligation and the combination of the two) resulted in a significant increase in fecal excretion of hexachlorobenzene. Moreover, the combination of hexadecane and bile duct ligation produced a greater increase in fecal excretion of hexachlorobenzene in blood, fat and kidney were not affected by any of the treatments, but liver concentrations were reduced significantly by bile duct ligation. Concentrations of hexachlorobenzene in intestinal contents indicate that intestinal-wall passage is the primary route of elimination from the body and that enhancement of elimination occurs mostly distal to the jejunum.

Effects of lipids on bioavailability of sulfisoxazole acetyl, dicumarol, and griseofulvin in rats

AbstractThe effects of hexadecane, oleyl alcohol, polysorbate 80, trioctanoin, and triolein on the bioavailability of sulfisoxazole N1‐acetyl, dicumarol, and griseofulvin were investigated. Compared to administration of the drugs in water, the rate of absorption of the drugs was either decreased or not changed by the lipids. The extent of absorption of sulfisoxazole acetyl and dicumarol was significantly increased by polysorbate 80 and triolein and not affected by hexadecane or oleyl alcohol. Trioctanoin increased the extent of absorption of sulfisoxazole acetyl but had no effect on the absorption of dicumarol. Compared to the aqueous vehicle, the extent of absorption of griseofulvin was decreased by hexadecane, oleyl alcohol, and triolein, increased by polysorbate 80, and not affected by trioctanoin. The extent of absorption of sulfisoxazole acetyl was not affected by the amount of triolein in which it was administered nor by emulsification of triolein prior to administration.