Search PubMed⌕ Search

Biomedical subjects

G F Carl

Publications and source records attributed to G F Carl.

45 records · Page 3Linked to original sources
PubMedDate not supplied

Lipid peroxidation and antioxidant vitamins prior to, during, and after correction of diabetic ketoacidosis.

Oxidative stress plays an important role in the chronic complications of insulin-dependent diabetes mellitus (IDDM). Hyperketonemia, as well as hyperglycemia, is involved in the generation of oxygen-free radicals. We have studied the degree of oxidative stress in six patients before, during, and after correction of diabetic ketoacidosis (DKA) by determining the plasma ratios of C20 and C18 fatty acids to C16 fatty acids in the cholesteryl esters of the lipoproteins as well as in the plasma concentrations of the antioxidant vitamins A, C, and E. Lipid peroxidation was slightly increased prior to treatment. However, the C20/C16 ratio at 120 h was significantly decreased in comparison to the ratio at pretreatment (P<.025), at 6-8 h (P<.005), and at 24 h (P<.025). The C18/16 ratio at 120 h was also decreased in comparison to the ratio at 6-8 h (P<.025), indicating an increase in lipid peroxidation after correction of DKA. Vitamin A was below normal at pretreatment and was increased at 120 h (P<.05). Vitamin C was normal at pretreatment and decreased to low normal at 24 h (P<.005). Vitamin E was normal at pretreatment and decreased to below normal at 24 and 120 h, although the changes were not statistically significant. These data demonstrate that there is an increase in lipid peroxidation after the correction of DKA and therefore support the position that administering antioxidant vitamins during the treatment of DKA could be beneficial in minimizing oxidative stress and possibly both the acute and chronic complications of IDDM.

Adolescent↗
PubMedDate not supplied

Diabetic ketoacidosis depletes plasma tryptophan.

Diabetic ketoacidosis (DKA) is a severe metabolic disturbance of insulin-dependent diabetes mellitus (IDDM) which has a significant effect on amino acid metabolism. Amino acids serve as precursors for various neurotransmitters which are involved in affective disorders, and patients with IDDM are known to have an increased prevalence of affective disorders. We monitored the plasma concentrations of 23 amino acids in six adolescents prior to treatment of DKA and at 6, 24 and 120 hours after initiation of treatment. The well-known increase in the concentrations of the glucogenic amino acids and the decrease in the branched-chain amino acids were observed in response to treatment of DKA. Low levels of tryptophan were found prior to treatment of DKA. Treatment increased the plasma tryptophan levels, but the mean concentration remained low throughout the sampling period. Only the glutamate-derived amino acids (glutamate, proline and glutamine) from the Krebs cycle pool were significantly affected by treatment. Glutamine declined initially, but recovered as the plasma pH normalized. Our results indicate that DKA causes a depletion of plasma tryptophan. This depletion may predispose some patients with IDDM to have affective disorders secondary to a neurotransmitter imbalance.

Adolescent↗
PubMedDate not supplied

Chronic carbamazepine treatment in the rat: efficacy, toxicity, and effect on plasma and tissue folate concentrations.

Folate depletion has often been a problem in chronic antiepileptic drug (AED) therapy. Carbamazepine (CBZ), a commonly used AED, has been implicated in some clinical studies. A rat model was developed to examine the effects of chronic CBZ treatment on folate concentrations in the rat. In the course of developing this model, a common vehicle, propylene glycol, by itself in high doses, was found to exhibit protective properties against induced seizures and inhibited weight gain. Seizures induced by hexafluorodiethyl ether (HFDE) were also found to be a more sensitive measure of protection by CBZ than seizures induced by maximal electroshock (MES). Oral administration of CBZ as an aqueous suspension every 8 h at a dose of 250 mg/kg was continuously protective against HFDE-induced seizures and was minimally toxic as measured by weight gain over 8 weeks of treatment. The CBZ levels measured in plasma and brain of these animals, however, were below those normally considered protective. This treatment with CBZ had no apparent adverse effect on folate concentrations in the rat, and, indeed, the folate concentration increased in liver after 6 weeks of treatment and in plasma at 8 weeks of treatment.

Aging↗
PubMedDate not supplied

Genetically epilepsy-prone rats are characterized by altered tissue trace element concentrations.

Since trace element abnormalities have been found in the human epileptic population, trace element concentrations were determined in blood and tissues of genetically epilepsy-prone rats both exposed to an unexposed to seizure-inducing stimuli and in genetically related epilepsy-resistant rats. Half of the epilepsy-prone group were exposed to seizure-inducing sound twice daily for 3 weeks. Food intake and weight gain were monitored for each animal. Genetically epilepsy prone rats with induced seizures consumed significantly less food and gained less weight than did the epilepsy resistant group. Seizure prone rats without seizures consumed the same amount of food as the resistant rats but gained less weight than the resistant strain but more than the seizure-induced animals. Epilepsy-prone animals had significantly altered trace element concentrations in tissues as compared with the resistant animals independent of seizure induction. Brain and liver iron, liver copper, and brain and heart manganese levels were all significantly lower in the seizure-prone rats as compared with the seizure-resistant rats. In the seizure-prone rats, induction of seizures resulted in an increase in brain and heart zinc levels and a decrease in whole blood manganese levels. These results demonstrate that both genetic factors relevant to susceptibility to seizures and the seizures themselves are associated with changes in trace element concentrations.

Acoustic Stimulation↗
PubMedDate not supplied

Phenytoin-folate interactions: differing effects of the sodium salt and the free acid of phenytoin.

Chronic phenytoin (PHT) treatment has long been associated with folate deficiency. It has been suggested that pH changes in the gut associated with PHT ingestion may be responsible for decreased folate uptake either by direct inhibition of folate transport into the intestinal mucosa or by inhibition of folate conjugase activity. To examine these possibilities, rats were gavaged chronically with PHT using either the sodium salt (NaPHT) or the free acid (HPHT) in the presence of folic acid as the dietary source of folate. The NaPHT caused a greater depletion of folate in the liver and brain and a significant increase in methylenetetrahydrofolate reductase activity in the liver. The HPHT caused a significantly decreased weight gain over the 8 weeks of treatment and resulted in a much higher liver PHT concentration and a slightly lower plasma PHT concentration. These data support the hypothesis that PHT-induced changes in pH in the gut affect the enterohepatic circulation of folate.

Animals↗
PubMedDate not supplied

Manganese and epilepsy: brain glutamine synthetase and liver arginase activities in genetically epilepsy prone and chronically seizured rats.

Low blood manganese (Mn2+) concentration is associated with epilepsy in humans and rats. The low Mn2+ concentration is attributed by some investigators to the seizure activity associated with the epilepsy, whereas others propose that the low Mn2+ concentration may be secondary to genetic mechanisms underlying the epilepsy. To begin to differentiate between these possibilities, Mn(2+)-binding enzymes of liver and brain (i.e., arginase and glutamine synthetase, respectively) were assayed in rats exposed to chronically induced seizures and in genetically epilepsy-prone rats (GEPRs). Chronic seizures caused a decrease in whole blood Mn2+ levels but did not affect brain Mn2+ concentrations. Arginase activity was increased in livers of rats with chronic seizure as compared with controls, but this difference was eliminated when Mn2+ was added to the assay. Brain glutamine synthetase activity was unaffected by chronic seizures, but the activity of this enzyme was significantly lower in GEPR brain than in control brain. Liver arginase activity tended to be lower in GEPRs, although the difference was not statistically significant. These data indicate that seizures affect liver arginase activity through changes in liver Mn2+ concentration, but GEPRs show abnormalities in Mn(2+)-dependent enzymes apparently independent of seizure activity.

Animals↗