The influence of proline and lysine solution ingestion on ethanol metabolism after chronic oral ethanol administration was investigated in stroke-prone spontaneously hypertensive rats (SHRSP). Compared with rats that were not administered ethanol (control group), the prolonged ethanol-administered rats (EtOH group) showed little change in their blood ethanol levels, but a remarkable increase and slow appearance in the blood acetaldehyde levels after the oral administration of ethanol. When prolonged ethanol-administered rats ingested the proline solution (EtOH/Pro group), higher levels of blood ethanol continued. However, the increase in blood acetaldehyde levels was not observed in the EtOH/Pro group. In the case of prolonged ethanol-administered rats that ingested the lysine-containing solution (EtOH/Lys group), blood ethanol levels decreased and disappeared 4h after the oral administration. An effect of lowered blood acetaldehyde levels was also observed. When prolonged ethanol-administered rats ingested both proline and lysine (EtOH/Pro+Lys group), the effect on blood ethanol levels was similar to that of rats that had ingested lysine only, and the influence on blood acetaldehyde was like that of rats that had only ingested proline. These results suggest that proline and lysine can regulate ethanol metabolism and the influence of proline on ethanol metabolism is different from that of lysine.
Astaxanthin, one of the naturally occurring derivatives of vitamin A, was found to suppress lipid peroxidation in a rat liver microsomal system. This substance was also found to suppress lipid peroxidation in rats induced by either carbon tetrachloride or 60Co-irradiation. The suppressive effect of astaxanthin on lipid peroxidation was more potent than that of α-tocopherol.
Ethanol feeding daily for 40 days to rats enhanced cholesterol, triglycerides, phospholipids (PL), and glycolipids contents of intestinal brush borders. The observed increase in membrane PL was reflected in phosphatidyl serine, phosphatidyl inositol, phosphatidyl choline, and phosphatidyl ethanolamine. Feeding of an 8% protein (low protein; LP) diet to rats reduced the cholesterol content but augmented PL, triglyceride, and cerebroside contents of brush borders compared with the control values. Membranes from ethanol-fed, malnourished animals revealed a decrease in membrane PL and triglyceride contents compared with those values for LP-fed rats. Feeding of a 30% protein (high protein; HP) diet to rats significantly increased various lipid fractions (cholesterol, PL, cerebrosides, and gangliosides) of intestinal microvillus membrane (MVM) compared with those of the controls. Ethanol administration together with the HP diet reduced membrane cholesterol, PL, triglycerides and glycolipids contents compared with those values for HP-fed animals. Thus, the feeding of a HP diet prevented the lipid accumulation in the rat intestine induced by chronic ethanol feeding. These results suggest that lipid composition of intestinal MVM is modified by ethanol and dietary protein regimens. The sensitivity of MVM lipid composition to ethanol is influenced by the dietary protein content of the animals.
The effect of iron deficiency on the activities of xenobiotic metabolizing enzymes, both activating (Phase I) and conjugating (Phase II), was studied in an experimental system. A group of male weanling Fischer rats was fed a casein sucrose starch-based diet devoid of iron for a period of 6 weeks. Another group of rats, which received an iron-sufficient diet, was used as the control. Hematological investigations on hemoglobin, protoporphyrin/heme ratio, and serum iron confirmed the development of iron deficiency in the experimental group by 6 weeks. At the end of the experimental period, microsomes and cytosolic preparations were made from various tissues that are sites of drug metabolism, i.e., liver, kidneys, lungs, and intestinal mucosa. Activities of many enzymes of Phase I, like cytochrome P-450, aryl hydrocarbon hydroxylase, aminopyrine demethylase, aniline hydroxylase and microsomal epoxide hydrolase and of Phase II, like uridine diphosphoglucuronyl transferase and glutathione-S-transferase, were investigated. The results showed that the activities of aminopyrine demethylase, aniline hydroxylase, and microsomal epoxide hydrolase among the activating enzymes and uridine diphosphoglucuronyl transferase, a conjugating enzyme, were significantly decreased in iron deficiency. An impairment in detoxification of ingested xenobiotics is thus indicated in iron deficiency. This might lead to the persistence of ingested compounds in the body without elimination, which might prove to be harmful to the host. Formation of electrophilic metabolites without subsequent removal may result in the formation of DNA adducts, which is a necessary step in chemical carcinogenesis.
Protein catabolism and the elimination of urea nitrogen increase in the diabetic condition. The mechanism involved in these increases was clarified by studying the levels of enzymes connected to the urea cycle. As vanadium in the form of sodium orthovanadate has been shown to possess insulin-like properties, its effect on urea-cycle enzymes were studied. Male Wistar rats were made diabetic by streptozotocin, and the diabetic rats were then treated with sodium orthovanadate for 15 days. The altered blood glucose, urea, and activities of liver urea-cycle enzymes such as ornithine transcarbamoylase, arginosuccinase, arginase, aspartate transaminase, and alanine transaminase seen in the diabetic rats were found to be normalized in the sodium orthovanadate-treated diabetic animals. These results indicate the beneficial effect of sodium orthovanadate on experimental diabetes.
In this study the level of some of the extracellular antioxidant proteins were investigated in 14 marasmic (M), 19 kwashiorkor (KWO), and 9 healthy children. Weight/age (W/A) and length/age (H/A) were assessed for each child. Serum level of each of ferritin, transferrin, ceruloplasmin, haptoglobin, hemopexin, and albumin were determined. W/A and H/A z-scores for both M and KWO children were less than -4.0, whereas those for healthy children were normal for weight (<-1.65) but less than -2.0 for the length. Mean serum ferritin level was significantly increased above the normal level for both M and KWO groups. Mean serum levels of the other five proteins were significantly reduced in KWO children. In M children, the mean level of each of transferrin, ceruloplasmin, and albumin was reduced but was still significantly higher than that in KWO children. By Pearson correlation analysis, serum albumin in both M and KWO children was highly significantly correlated with weight as well as with each of serum transferrin, ceruloplasmin, hemopexin, and haptoglobin.
ADP-induced platelet aggregation of normal individuals and of patients with unstable angina were studied. Abnormalities of platelet function included increased aggregability. The ADP concentration required for half-maximal aggregation was significantly lower (4.28±0.30μM) in the unstable angina patients compared with that for normal individuals (5.24±0.15μM). The results are suggestive of platelet aggregation as a useful prognostic indicator for unstable angina.
The pancreatic function diagnostant (PFD test) and fecal chymotrypsin test were performed simultaneously in patients after pancreatic surgery, and findings for both tests were analyzed. The p-aminobenzoic acid recovery rate in the PFD test and the chymotrypsin activity in stools decreased after pancreatectomy, particularly after extended radical pancreaticoduodenectomy. Chymotrypsin activity in stools, measured by the fecal chymotrypsin test after extended radical pancreaticoduodenectomy, was significantly lower than the normal level. The D-xylose output in the extended radical group was significantly (p<0.05) lower than that following conventional pancreaticoduodenectomy. The results allow the conclusion that the absorption factor must be taken into account when evaluating the pancreatic exocrine function by the PFD test.