The mechanism of initiation of lipid peroxidation in rat liver mitochondria in the resting state by iron chelates of adenine nucleotides has been investigated. ADP was required at three times the concentration of Fe2+ for formation of an active complex and at ten times the concentration of Fe2+ for maximal activity to induce lipid peroxidation. Iron chelates with ATP showed as high activity as those with ADP for initiation of peroxidation, but those with AMP showed low activity. ADP-Fe3+, prepared from ADP and Fe(NH4)(SO4)2, did not induce mitochondrial lipid peroxidation, whereas ADP-Fe2+, prepared by incubation of ADP with FeSO4, oxidized to form a Fe3+-type complex, as characterized by spectroscopic analysis, did induce lipid peroxidation. The oxidation of ADP-Fe2+ to an ADP-Fe3+-type complex with associated oxygen uptake suggested the formation of an ADP-Fe3+-oxygen complex capable of initiating lipid peroxidation. The molar ratio of Fe3+ formation to oxygen uptake was approximately 2.5 on incubation of Fe2+ with ADP. The process of ADP-Fe2+-induced lipid peroxidation did not involve superoxide, H2O2, or the OH-radical, because it was not inhibited by superoxide dismutase, catalase, or mannitol, an OH-radical scavenger.
In order to investigate the physiological action of Polydextrose as a dietary fiber, we fed rats 3% Polydextrose diet containing either pectin or cellulose for 15 days. The effects of Polydextrose on fecal weight and gastrointestinal transit time were observed, and digestibility and the inhibitory effect of the fiber on intestinal digestive enzymes were examined. Polydextrose was partially hydrolyzed by rat intestinal mucosal homogenate, and liberated glucose increased depending on incubation time. However, Polydextrose had no inhibitory effect on the activity of disaccharidases. The combination of Polydextrose and either pectin or cellulose significantly increased fecal weight and evidently shortened transit time. The effect of Polydextrose supplementation on tissue weight was found in the cecum only, and not in other tissues. The concentration of serum constituents such as total and free cholesterol, triacylglycerol, phospholipid, and glucose was not affected by Polydextrose ingestion. These results suggest that Polydextrose partially demonstrates the dietary fiber actions such as increase in fecal volume and weight, shortening of transit time, and softening of feces.
In dog heart mitochondria, the total flavin content was found to be higher in intermyofibrillar mitochondria (0.88 nmol per mg protein for FAD, 0.10 for FMN) than in subsarcolemmal mitochondria (0.27 for FAD, 0.07 far FMN). Sixty-minute occlusion of the coronary artery led to a decrease in FAD content in the ischemic region by approximately one-third. Glutathione reductase activity in subsarcolemmal mitochondria was depressed significantly by Ischemia. The activity coefficient increased to 1.36 from the control (1.07). Our results indicate that depletion of riboflavin content in mitochondria may be related to various metabolic alterations under ischemia and that riboflavin in subsarcolemmal mitochondria is influenced more by ischemia than that in intermyofibrillar ones.
It has been previously shown that plasma vitamin A concentration was decreased in both diabetic patients and streptozotocin diabetic rats. In the present study the effect of insulin administration to streptozotocin diabetic rats on plasma and liver vitamin A levels was determined. The daily insulin treatment began 3 weeks after the animals had been made diabetic and continued for 3 weeks. Plasma vitamin A levels were significantly lower in the diabetic rats than in the nondiabetic controls. In the insulin-treated diabetic rats, the plasma vitamin A together with the plasma glucose reverted to the control levels. Livers from the insulin-treated diabetic animals stored vitamin A in about the same amounts as did the livers of the untreated group but significantly more than those of the nondiabetic controls. The liver stores of vitamin A seem to reflect the amount of vitamin A consumed. These results demonstrate that treatment of diabetic rats with insulin restores plasma vitamin A to normal levels. However, the mechanism by which it does so remains to be determined.
Plasma amino acids were analyzed in three patients with myotonic dystrophy, and the therapeutic effect of taurine, a cell membrane-stabilizing agent, on plasma amino acids and clinical data were analyzed. Pretreatment plasma amino acid analysis in the three cases revealed a decreased level of methionine compared to levels in healthy controls. In Case 1, taurine administration resulted in a further decrease in methionine levels. We were unable to demonstrate any improvement in clinical symptoms.
In 15 patients with IgA nephropathy, we studied Cu, Zn-SOD localization in glomeruli by immunohistochemistry, and examined the correlation of the clinical findings with the intensity and location of Cu, Zn-SOD specific staining. In healthy controls, Cu, Zn-SOD was localized in tubules and not in glomeruli. In IgA nephropathy, the enzyme was detected in the glomeruli of 13 out of 15 patients. An inverse correlation was observed between Cu, Zn-SOD stainability and the serum creatinine level. Negative correlation was also observed between Cu, Zn-SOD stainability and the histological grade of sclerosis in IgA nephropathy. We conclude that the study of Cu, Zn-SOD stainability in glomeruli is useful to assess the prognosis in IgA nephropathy.
Preterm infants are particularly at risk of copper deficiency but there is no method for assessing copper status in preterm infants that has been unequivocally accepted. We explored the potential value of assays of erythrocyte copper concentration and erythrocyte superoxide dismutase (SOD) activity. Erythrocyte copper was measured by continuous nebulization flame atomic absorption spectrophotometry using a slotted tube atom trap. Erythrocyte SOD activity was measured by an automated method based on the inhibition of pyrogallol autoxidation. The methods gave reproducible results and the sample volumes were small. Due to the high frequency of blood transfusions, only 38% of the infants investigated had any results for erythrocyte copper or SOD that were considered to be unaffected by transfusion. Compared with adults, there appeared to be a difference in the distribution of copper in the erythrocytes of the small group of infants whose erythrocyte biochemistry was unaffected by blood transfusion. We conclude that neither erythrocyte copper nor erythrocyte SOD is likely to be of much value in assessing copper status in preterm infants.