Blood glycated hemoglobin concentration reflects long-term serum glucose levels in dogs. In this study, the effects of several diseases on blood glycated hemoglobin levels have been evaluated. For this study, blood samples were drawn from 93 unhealthy dogs. The animals were distributed into 10 groups according to pathological process (group 1, digestive problems; group 2, leishmaniasis; group 3, anemia; group 4, dermatological disorders; group 5, urinary problems; group 6, cardiorespiratory problems; group 7, diabetes mellitus; group 8, insulinoma; group 9, general diseases; group 10, control group). Blood glucose and glycated hemoglobin concentrations and hemoglobin and hematocrit values were analyzed in all the animals. In diabetic dogs, a strong increase in blood glycated hemoglobin was observed when compared with the other groups (P < 0.01). In contrast, dogs with insulinoma showed a decrease in blood glycated hemoglobin, though significant differences were not reported in all cases. No change in blood glycated hemoglobin concentrations were reported in dogs affected by other diseases. So, we can suppose that only the chronic alterations in glucose metabolism (chronic hyper- or hypoglycemia) can induce significant changes on the blood glycated hemoglobin concentrations in dogs.

We have investigated the accumulation of diacylglycerol (DAG) induced by carbon tetrachloride (CCl4)-derived radicals in the liver of female Sprague-Dawley (SD) rats after intraperitoneally injecting CCl4. DAG is an intracellular activator of protein kinase C (PKC) which regulates cell proliferation and differentiation. The electron spin resonance (ESR) study gave the signal of the PBN-CCl3 adduct in the liver of the rats which were pretreated with PBN, confirming that CCl4 was metabolized into CCl3-radicals with cytochrome P450 enzyme and indicating that PBN could trap them. The blood biochemical assay supported the trapping of the CCl3-radicals; the pretreatment of rats with PBN inhibited the increase in the GOT and GPT values upon exposure to CCl4. The Fourier transform-infrared (FT-IR) study indicated in comparison with the model compounds that the CCl4-injected rats accumulated DAG in addition to phosphatidylcholine, phosphatidylethanolamine and triglyceride (TG) in the lipid membrane fraction of the liver homogenate. DAG was found to be ca. 10-15% of the membrane phospholipids by weight. However, DAG was not found in the lipid of the liver microsomes, suggesting that it is formed only in the cell membrane of liver. Also, neither DAG nor TG was found in the lipid membrane of the rats that were pretreated with PBN followed by an injection of CCl4. The formation of DAG was confirmed by an HPLC study. The activation of PKC was observed in liver homogenate in the rats that were injected with CCl4. On the basis of the above findings, it was concluded that the CCl4-derived radicals stimulate PKC through the accumulation of DAG in the liver membrane of the rats. Furthermore, it was shown that PBN has a protective and therapeutic effect against CCl4-induced damage

FT-IR and ESR were used for on the investigation of the CCl4-induced peroxidation of rat liver microsomes in combination with biochemical methods. Lipid peroxidation was assayed by TBA reagent in the presence of CCl4 and NADPH. The CCl3 - radical was detected by ESR spectroscopy with a spin trapping reagent of PBN. The FT-IR spectroscopy revealed that absorption band of -C-H in -C=C-H decreased in intensity at 3012 cm(-1), but the absorption bands of the phosphate head and choline in the phospholipids did not significantly change between 1300 and 900 cm(-1). These findings were interpreted to be due to the removal of H- from -C=C-H by radicals as the first step of lipid peroxidation, and to the absence of dephosphorylation of phospholipids in the microsomal membrane. This is the first IR spectroscopic evidence indicating the nature of damage to a microsomal membrane caused by CCl4 treatment. The spectroscopies used here demonstrated that they are useful tools to observe the damage

This study revealed the dose dependency of prednisolone tertiary-butylacetate (PTBA) treatment on the establishment of Echinococcus multilocularis in the small intestine of Mongolian gerbil (Meriones unguiculatus) and that some of the physiological parameters of host were correlated with the doses of PTBA and establishment of the worm. Twenty Mongolian gerbils were divided into 5 groups, according to the doses of PTBA; 0 mg, 0.5 mg, 2 mg, 5 mg and 10 mg per head. All animals were injected intraperitoneally with PTBA every other day from 6 days before to 6 days after infection. Doses of PTBA and the number of worms recovered at 7 days post-infection showed a positive correlation (r=0.929, P0.0001). The increase of total protein (TP) and the decrease of the percentage of lymphocytes in the peripheral leukocytes were dependent on doses of PTBA (TP: r

We evaluated the expression of parathyroid hormone-related protein (PTHrP) by immunohistochemistry in eight benign and malignant mammary mixed tumors of dogs with (n = 4) and without (n = 4) hypercalcemia. Positive immunoreactive staining for PTHrP was observed in all four tumors from hypercalcemic dogs. The mammary tumors from 2 of the 4 normocalcemic dogs stained positively for PTHrP, but the numbers of immunoreactive cells and intensity of the immunoreaction were less than in the hypercalcemic dogs. In the other 2 tumors without hypercalcemia, the tissue samples were negative for PTHrP