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PubMed1990

2-Mercaptoacetate stimulates sham feeding in rats.

Rats maintained on a LF diet (Purina chow) were pretreated with 0.3 M/kg 2-mercaptoacetate, an antagonist of B-oxidation of fatty acids, 60 min before sham feeding condensed milk with open gastric cannulas. 2-Mercaptoacetate significantly increased 30-min milk intake by about 35%. This suggests that blockade of fatty acid oxidation 1) participates control of feeding even in rats adapted to low fat diets, and 2) modulates not only the timing of meal initiation as previously reported by others, but also may influence the rate of ingestion and/or meal size. Finally, 2-mercaptoacetate pretreatment did not block the synergistic inhibition of sham feeding elicited by simultaneous injections of glucagon and cholecystokinin.

Animals↗
PubMedDate not supplied

Conditioned taste aversion produced by inhibitors of fatty acid oxidation in rats.

The aversive effects of mercaptoacetate (MA) and methyl palmoxirate (MP) were examined in the present experiment. We used a conditioned taste aversion (CTA) paradigm for Sprague-Dawley rats maintained on a low- or high-fat diet, and determined that MA and MP both produce profound aversions to a novel saccharin solution. Because it is known that the stimulation of food intake brought about by MA administration is blocked by destruction of vagal afferents. we repeated the CTA experiment in control and capsaicin-treated rats. Results show that although the capsaicin-treated rats did not increase food intake after MA administration, the CTA produced by MA remained. Therefore, the neural pathways for the aversive and orexigenic effects of MA are distinct. We conclude that MA and MP are aversive, and that the aversive signal generated by MA does not involve vagal afferents or other fibers damaged by capsaicin.

Animals↗
PubMed2002

Effects of 2-mercaptoacetate on ingestive behavior in 18- and 21-day-old rats.

Previous work has demonstrated that mercaptoacetate (MA), which interferes with oxidation of fatty acids, can produce increases in intake in both adult and preweanling rats between 12 and 15 days of age. In both pups and adults, the increased intake is related to a decrease in the latency to initiate intake, but the duration of the effects of MA and the effective doses of MA differ in young pups compared to adult rats. Thus, in the present experiments, we examined older pups to determine the effects of administration of MA on ingestive behavior and energy-related markers (blood glucose, free fatty acids, and beta-hydroxybutryrate levels and weight loss) during the weaning transition. Pups aged 18 or 21 days received an i.p. injection of a 0, 22.8, 45.6 or 68.4 mg/kg MA, and after 1 h consumed a milk diet from the floor of a test container. Unlike younger pups or adult rats, MA did not stimulate intake in 18- or 21-day-old pups in a 30 or 60 min test, instead, the higher doses significantly suppressed intake. In addition, while latency to initiate intake was not reduced, primarily due to the very short latencies observed in control pups, the duration of intake was decreased by the higher doses of MA. Finally, MA did produce changes in fatty acid oxidation in pups at both ages, but baseline levels of free fatty acids and beta-hydroxybutryrate differed across the ages, as did the pattern of changes produced by MA. The results suggest that in contrast to the effects observed in both younger pups and adult rats, during the early weaning period exogenous alterations of fatty acid oxidation fail to stimulate intake. In addition, similar to effects seen in young pups, high doses of MA can significantly suppress intake. These differences in responding to MA during the weaning period may reflect heightened sensitivity to similar signals produced endogenously as a result of developmental changes in diet and/or metabolism or may result from heightened sensitivity to aversive properties of administration of MA.

3-Hydroxybutyric Acid↗
PubMed2002

Effects of acute inhibition of fatty acid oxidation on latency to seizure and concentrations of beta hydroxybutyrate in plasma of rats maintained on calorie restriction and/or the ketogenic diet.

The present study was designed to evaluate the effects of acute inhibition of fatty acid oxidation on plasma levels of beta hydroxybutyrate and latency to PTZ-induced seizures in ad libitum- (AL), calorie-restricted normal rodent chow- (CR), and calorie-restricted ketogenic diet (KD)-fed young rats. Young (day 23) Sprague-Dawley rats were fasted for 8 h and then fed their respective diets for 21 days. On day 21 of the diet rats in each group received either saline or the fatty acid oxidation inhibitor mercaptoacetate (MA; 46 mg/kg intraperitoneally (i.p.). Two hours later, all rats received pentylenetetrazole (PTZ; 10 mg/kg; i.p.) every 10 min until seizure onset. Results demonstrated that KD-fed rats had the longest (P<0.05) latency to PTZ-induced seizures. KD-fed rats administered an acute dose of MA had lower (P<0.01) levels of beta hydroxybutyrate in plasma and shorter latency to PTZ-induced seizures compared with control KD-fed rats. However, there was not a significant positive correlation (P>0.10) between plasma beta hydroxybutyrate and latency to seizure, suggesting that beta hydroxybutyrate may be indirectly involved in the antiseizure effects of the KD. Fatty acid oxidation inhibition represents an experimental manipulation that may allow for more precise establishment and evaluation of levels of beta hydroxybutyrate in plasma necessary for antiseizure effects of the KD.

3-Hydroxybutyric Acid↗
PubMed1988

Optimization of efficiency in the glyoxalase pathway.

A quantitative kinetic model for the glutathione-dependent conversion of methylglyoxal to D-lactate in mammalian erythrocytes has been formulated, on the basis of the measured or calculated rate and equilibrium constants associated with (a) the hydration of methylglyoxal, (b) the specific base catalyzed formation of glutathione-(R,S)-methylglyoxal thiohemiacetals, (c) the glyoxalase I catalyzed conversion of the diastereotopic thiohemiacetals to (S)-D-lactoylglutathione, and (d) the glyoxalase II catalyzed hydrolysis of (S)-D-lactoylglutathione to form D-lactate and glutathione. The model exhibits the following properties under conditions where substrate concentrations are small in comparison to the Km values for the glyoxalase enzymes: The overall rate of conversion of methylglyoxal to D-lactate is primarily limited by the rate of formation of the diastereotopic thiohemiacetals. The hydration of methylglyoxal is kinetically unimportant, since the apparent rate constant for hydration is (approximately 500-10(3))-fold smaller than that for formation of the thiohemiacetals. The rate of conversion of methylglyoxal to (S)-D-lactoylglutathione is near optimal, on the basis that the apparent rate constant for the glyoxalase I reaction (kcatEt/Km congruent to 4-20 s-1 for pig, rat, and human erythrocytes) is roughly equal to the apparent rate constant for decomposition of the thiohemiacetals to form glutathione and methylglyoxal [k(obsd) = 11 s-1, pH 7]. The capacity of glyoxalase I to use both diastereotopic thiohemiacetals, versus only one of the diastereomers, as substrates represents a 3- to 6-fold advantage in the steady-state rate of conversion of the diastereomers to (S)-D-lactoylglutathione.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Electrolytic O-demethylation of methoxycatecholamines.

Electrolysis of 3-methoxycatecholamines in physiological solutions resulted in the formation of the parent catecholamines and their oxidation products. Conversion occurred at the anode. Maximal catecholamine production occurred in the presence of ascorbic acid.

Animals↗
PubMed1963

INACTIVATION OF THE RADIATION-RESISTANT SPOILAGE BACTERIUM MICROCOCCUS RADIODURANS. II. RADIATION INACTIVATION RATES AS INFLUENCED BY MENSTRUUM TEMPERATURE, PREIRRADIATION HEAT TREATMENT, AND CERTAIN REDUCING AGENTS.

The R(1) strain of Micrococcus radiodurans, previously determined to be more resistant than three other strains exposed to gamma radiation, was studied further to determine the influence of certain environmental factors on resistance to radiation inactivation. The frozen state offered insignificant protection to the organisms irradiated in raw puréed beef. Resistance was reduced by higher menstruum temperatures (40 and 50 C) during irradiation. Preirradiation heat treatment was found to lower resistance to subsequent irradiation. When the cells were irradiated in buffer at pH 5, 7, or 9, no differences in resistance were noted. Cell suspensions in buffer were protected to some extent by cysteine but not by thioglycolate. Ascorbate enhanced radiation inactivation.

Animals↗
PubMed1990

Brain glucoprivation and ketoprivation do not promote ingestion in the suckling rat pup.

We examined the possibility that brain glucose or ketone availability may control suckling or precocious feeding in the preweanling rat. Brain glucoprivation induced by 5-thio-D-glucose injection into the 4th ventricle did not increase feeding on orally infused milk until 30 days of age, although hyperglycemia was evoked as early as 9 days by the same treatment. Plasma ketone levels varied with suckling status, but pharmacological blockade of hepatic free fatty acid oxidation, which restricts ketone availability (ketoprivation), failed to increase suckling. Because the suckling rat can switch energy substrates under nutritional duress, we combined glucoprivation and ketoprivation. Feeding was suppressed, and suckling was not affected. Finally, we injected ketones into the 3rd brain ventricle and found that they increased feeding. Thus, in contrast to the adult rat, reduced glucose or ketone utilization by the brain does not increase food intake in the preweanling, but increased circulating and brain ketone concentrations may arouse feeding.

Animals↗
PubMed1983

Lack of a T-cell dependent subpopulation of macrophages in (dichloromethylene) diphosphonate-treated mice.

In Cl2MDP-osteopetrotic mice, one subpopulation of thioglycollate-induced peritoneal exudate macrophages (M phi) is missing. This subpopulation is precisely the one whose differentiation is known to be dependent on T-lymphocytes, as it is also missing in the athymic nu/nu mice. Cl2MDP-induced osteopetrosis being partially attributable to deficient osteoclastic bone resorption, raises the possibility that this missing M phi subpopulation might represent the precursors of osteoclasts. It is suggested from this work that the interplays between T-cells and M phi, so well known in immunity and inflammation, may also be relevant to osteoclastic differentiation and therefore, to bone remodeling.

Animals↗
PubMed1998

Absence of relation between the expression of cyclooxygenase isoforms and the synthesis of prostaglandin E2 in resident and thioglycollate-elicited macrophages in rats.

Macrophages exudating into inflammatory sites (thioglycollate-elicited macrophages, TGM) have a diminished ability to synthesize prostaglandins (PG) as compared with resident peritoneal macrophages (RM). Constitutive expression of cyclooxygenase-1 (COX-1) was lower in TGM than in RM but the releasability of arachidonic acid was not significantly different. Thus, the differences in expression of COX-1 were primarily responsible for the abilities of TGM and RM to synthesize PGE2 upon calcium ionophore (CaI) stimulation. COX-1 expression in RM and TGM was also correlated with their ability to synthesize PGE2 from exogenously added arachidonic acid. When exposed to lipopolysaccharide (LPS), the induction of COX-2 and the enhancement of PGE2 synthesis upon CaI were much lower in TGM as compared with RM the releasability of arachidonic acid upon CaI stimulation was relatively unchanged in RM but was reduced in TGM Thus, in TGM as compared with RM, a lower level of COX-1 expression and a lower level of COX-2 induction, and the reduction of arachidonate releasability by LPS exposure, are mainly responsible for lower PGE2 synthetic ability upon CaI stimulation. However, the different COX-2 induction by LPS in RM and TGM was not reflected in their increase in the ability to synthesize PGE2 from exogenously added arachidonic acid.

Animals↗
PubMed1981

Growth of bacteria and fungi in parenteral nutrition solutions containing albumin.

The ability of total parenteral nutrition (TPN) solutions containing albumin to support bacterial and fungal growth was studied. The following solutions were tested for microbial growth: (A) thioglycolate broth, (B) solution A with preservatives, (C) albumin 6.25 g in 500 ml 0.9% sodium chloride injections, (D) solution C with preservatives, (E) amino acid and dextrose TPN solution with magnesium sulfate and folic acid, (F) solution E with albumin 6.25 g in 500 ml, (G) amino acid and dextrose TPN solution with calcium gluconate and multivitamins, and (H) solution G with albumin 6.25 g in 500 ml. Each solution was inoculated with 1 X 10(5) bacteria/ml or 1 X 10(3) yeast/ml in 12 serial dilutions using minimum inhibitory concentration (MIC) plates. These were incubated at 37 degrees C for 48 hours, and cultures were visually rated on a scale of 0 (no growth) to 4 (maximal growth). Each culture was repeated for a total of 10 samples. Microbial growth was not affected by the low concentrations of preservatives available from the TPN additives. Undiluted TPN solutions were able to sustain fungal growth only. There was a significant increase in microbial growth in diluted TPN solutions containing albumin for S. aureus, C. albicans, T. glabrata, K. brier, S. marcescans, and E. coli. The presence of vitamins (solution G) impaired the ability of gram-negative bacteria to proliferate, and the addition of albumin (solution H) had no significant effect on the growth characteristics of the organisms in the solution. The presence of albumin had no effect on the growth of S. faecalis or Ps. aeruginosa. The addition of albumin to crystalline amino acid TPN solutions increases the potential of these solutions to support the growth of fungi and bacteria. Hence, it is recommended that albumin be administered separate from amino acid TPN solutions.

Albumins↗
PubMed1980

The guinea-pig: an animal model for human skin absorption of hydrocortisone, testosterone and benzoic acid?

14C ring-labelled hydrocortisone, testosterone and benzoic acid dissolved in acetone were applied to the backs of guinea-pigs (4 microgram/cm2). Percutaneous absorption was quantified by following the excretion of tracer in urine and faeces for 5 days. Absorption of hydrocortisone and benzoic acid was 2.4% (s.d. = 0.5; n = 3) and 31.4% (s.d. = 9.1; n = 3) of the applied dose respectively, similar to published human absorption data. Testosterone was absorbed to a greater extent in guinea-pigs (34.9% +/- 5.4; n = 5) than man. A thioglycollate based depilatory cream significantly increased the skin absorption of testosterone, while the absorption velocity was unaltered. Two analytical methods were compared, direct counting versus wet ashing; results were in the same range for the three compounds. Two methods of quantifying skin absorption were compared; urine recovery corrected for incomplete urinary excretion after parenteral administration versus the addition of urine and faecal recovery. For benzoic acid, excreted mainly in the urine (88.1%), the two methods gave similar results; for testosterone, excreted in the urine to a lesser extent (46.8%), the method of addition of urine and faecal recovery appeared to be more correct.

Animals↗
PubMed1978

Kinetics and mechanisms of macrophage activation by Corynebacterium anaerobium.

Kinetics and mechanisms of macrophage activation by heat-killed Corynebacterium anaerobium (CA) in mice were investigated. The carbon clearance test revealed that the function of the reticuloendothelial system rose markedly on the 4th day after a single intravenous injection of CA and continued in a highly enhanced state until the 14th day. This activity declined gradually and dropped to a normal level around the 21st day. On the other hand, both lysosomal enzymes, beta-glucuronidase and acic phosphatase, of peritoneal macrophages decreased after the CA injection and then recovered, taking an almost inverse course to the function of the reticuloendothelial system. These results might be attributable to possible extracellular secretion of the lysosomal enzymes in accordance with macrophage activation by CA. A remarkable cytotoxicity of peritoneal macrophages, examined in vitro against L 929 cells, was detected on the 4th day following intraperitoneal administration of CA. It was maintained up to the 14th day and then declined rapidly. The mechanisms of macrophage activation by CA were also examined in vitro. CA-homogenate, heat-killed CA disrupted with an ultrasonicator, directly activated thioglycollate-induced macrophages. The macrophages were aslo activated by simultaneous treatment with both CA-homogenate and CA-sensitized spleen cells. Furthermore, the supernatant obtained from the culture of CA-sensitized spleen cells with CA-homogenate was capable of inducing activation of the macrophages. Conversely, the culture supernatant of spleen cells from CA-immunized athymic nude mice with CA-homogenate was unable to activate them. It was ascertained from the above-mentioned results that macrophages are activated initially by direct action of CA in a nonspecific way and subsequently by a soluble factor elaborated by CA-sensitized lymphocytes in an immunological way.

Acid Phosphatase↗
PubMed1995

Regulation of neutral cholesterol esterase activity by phospholipids containing negative charges in substrate liposome.

The effect of phospholipids on cholesteryl ester hydrolysis by neutral cholesterol esterase in alveolar macrophages was studied. Among the phospholipids used as emulsifiers, those with a negative charge, such as phosphatidylserine, phosphatidic acid, phosphatidylinositol, and cardiolipin, gave a higher level of hydrolysis by neutral cholesterol esterase than other less negatively charged phospholipids, such as phosphatidylcholine, lysophosphatidylcholine, phosphatidylethanolamine, and sphingomyelin. Phospholipase D treatment of liposomes emulsified with phosphatidylcholine produced phosphatidic acid and enhanced cholesteryl ester hydrolysis. Phospholipase A2 treatment produced lysophosphatidylcholine and decreased the hydrolysis. The hydrolysis of cholesteryl ester in lipid droplets obtained from cholesterol-laden macrophages elicited by thioglycollate in the rat peritoneal cavity was low compared to artificial liposomes emulsified with phosphatidylcholine. The reason for this was speculated to be that lipid droplets were low in total phospholipids and poor in phospholipids with strong negative charges but rich in phosphatidylethanolamine and sphingomyelin. These results suggest that the polar heads of phospholipids may play an important role in cholesteryl ester hydrolysis by neutral cholesterolesterase.

Animals↗