Elevated Blood Glucose after Compound 48/80 Treatment Is Not Related to Hepatic Mast Cell Degranulation in Rats

Dimlich, Ruth V.W.; Reilly, Frank

doi:10.3181/00379727-183-42425

Cited by 4 publications

(2 citation statements)

References 28 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…(10) Furthermore, it has been shown that degranulation of mast cells existing in the liver tissue of rats treated once with C48/80 is not associated with glycogen depletion in the tissue. (11) Braun et al (12) have reported that depletion of reduced glutathione (GSH) induces glycogenolysis, resulting in stimulated VC synthesis in isolated mouse hepatocytes. Chan et al (13) have shown that glycogenolysis is involved in VC synthesis accompanied with GSH consumption in isolated rat hepatocytes.…”

Section: Introductionmentioning

confidence: 99%

Compound 48/80, a mast cell degranulator, causes oxidative damage by enhancing vitamin C synthesis via reduced glutathione depletion and lipid peroxidation through neutrophil infiltration in rat livers

Yashiro

Ohashi

et al. 2017

J. Clin. Biochem. Nutr.

View full text Add to dashboard Cite

In this study, we examined whether compound 48/80 (C48/80), a mast cell degranulator, causes hepatic oxidative damage in rats. Serum and liver biochemical parameters were determined 0.5, 3 or 6 h after a single treatment with C48/80 (0.75 mg/kg). Serum histamine and serotonin levels increased 0.5 h after C48/80 treatment but diminished thereafter. Increases in serum vitamin C (VC) and transaminases and hepatic hydrogen peroxide, lipid peroxide, and myeloperoxidase levels and a decrease in hepatic reduced glutathione level occurred 0.5 h after C48/80 treatment and further proceeded at 3 h, but these changes diminished at 6 h. Serum lipid peroxide and hepatic VC levels increased 3 h after C48/80 treatment. Hepatic glycogen level decreased 0.5 h after C48/80 treatment and further decreased at 3 h. Pre-administered ketotifen diminished all these changes found at 3 h after treatment, while pre-administered NPC 14686 diminished these changes except changes in serum histamine and serotonin levels. Hepatocellular apoptosis observed at 3 h after C48/80 treatment was attenuated by pre-administered ketotifen and NPC 14686. These results indicate that C48/80 causes oxidative damage by enhancing VC synthesis via reduced glutathione depletion-dependent glycogenolysis and lipid peroxidation through neutrophil infiltration following mast cell degranulation in rat livers.

show abstract

Section: Introductionmentioning

confidence: 99%

Compound 48/80, a mast cell degranulator, causes oxidative damage by enhancing vitamin C synthesis via reduced glutathione depletion and lipid peroxidation through neutrophil infiltration in rat livers

Yashiro

Ohashi

et al. 2017

J. Clin. Biochem. Nutr.

View full text Add to dashboard Cite

show abstract

“…because it provides an expedient method for measuring relative differences in circulating glucose in a large number of blood samples from a large number of rats. 41 …”

Section: Experimental Modelmentioning

confidence: 99%

Facilitating postischemic reduction of cerebral lactate in rats.

Dimlich

Nielsen

1992

Stroke

View full text Add to dashboard Cite

Background and Purpose: Dichloroacetate facilitates a decrease in brain lactate during reperfusion after incomplete ischemia. This study examined the possible activation of pyruvate dehydrogenase enzyme by dichloroacetate to explain this effect. Because the duration of ischemia and hyperglycemia exacerbate ischemic brain damage, the effect of both of these factors on lactate reduction with and without dichloroacetate treatment after ischemia also was explored.Methods: The two-vessel occlusion and controlled blood loss model of stroke was applied to anesthetized rats. Samples of cerebral cortex were analyzed for lactate by enzyme fluorometry and for pyruvate dehydrogenase activity by radioassay.Results: Treatment with dichloroacetate produced no significant stimulation of pyruvate dehydrogenase after ischemia. When the duration of ischemia was increased or 50% glucose was infused before ischemia, brain lactate was significantly higher (/?<0.01, Duncan's test). After 30 minutes of ischemia, treatment with a low dose of dichloroacetate (25 mg/kg) improved the reduction in lactate (p<0.01, Duncan's test).Conclusions: These results indicate that although dichloroacetate reduces brain lactate after cerebral ischemia, the mechanism of action does not involve dichloroacetate's known ability to stimulate pyruvate dehydrogenase. However, these data support the use of dichloroacetate to lower cerebral lactate, especially in cases where ischemia is >30 minutes in duration. They also suggest that early restoration and maintenance of perfusion after ischemia and discontinuing the use of 50% glucose before impending ischemia likewise would facilitate reduction of postischemic brain lactate. (Stroke 1992;23:1145-1153 KEY WORDS • cerebral ischemia • glucose • lactates • rats

show abstract

Physiological responses to central and peripheral injections of compound 48/80 and histamine in chicks

Tachibana

Hirai

Tomita

et al. 2019

Physiology & Behavior

View full text Add to dashboard Cite

Elevated Blood Glucose after Compound 48/80 Treatment Is Not Related to Hepatic Mast Cell Degranulation in Rats

Cited by 4 publications

References 28 publications

Compound 48/80, a mast cell degranulator, causes oxidative damage by enhancing vitamin C synthesis via reduced glutathione depletion and lipid peroxidation through neutrophil infiltration in rat livers

Compound 48/80, a mast cell degranulator, causes oxidative damage by enhancing vitamin C synthesis via reduced glutathione depletion and lipid peroxidation through neutrophil infiltration in rat livers

Facilitating postischemic reduction of cerebral lactate in rats.

Physiological responses to central and peripheral injections of compound 48/80 and histamine in chicks

Contact Info

Product

Resources

About