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PubMed1993

Sleep-wake disturbances in an animal model of chronic cholinergic insufficiency.

Rats reared on a diet in which choline is replaced with N-aminodeanol (NADE), undergo > 50% replacement of brain acetylcholine with acetylated NADE, a false cholinergic transmitter. We examined amounts of sleep and wakefulness in 7 littermate pairs of rats fed either NADE-substituted, or a choline control diet for > 100 days after weaning. During the lights-on portion of the 12/12 h light/dark cycle, NADE rats spent more time awake, and less time in both non-REM and REM sleep compared to littermate controls. Average durations of waking episodes were significantly increased in NADE rats. During the 12 h dark period, there were no between-group differences in sleep-waking amounts. Behavioral hyper-responsiveness which interferes with sleep onset, combined with reduced activity in brainstem cholinergic mechanisms involved in REM sleep generation may underlie daytime sleep-waking disturbances in NADE rats.

Acetylation↗
PubMed1987

Role of oxygen-derived free radicals in diet-induced hemorrhagic pancreatitis in mice.

The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis was studied by evaluating the effects of catalase, allopurinol, and dimethylsulfoxide on diet-induced acute hemorrhagic pancreatic necrosis in mice. The mortality rate and degree of hyperamylasemia associated with this model of pancreatitis were reduced by catalase but a similar result followed the administration of heat-denatured catalase, suggesting that the apparent protective effect of catalase was not the result of reductions in free radical levels. Neither allopurinol nor dimethylsulfoxide reduced mortality or degree of hyperamylasemia. The increased pancreatic content of amylase and the necrosis that characterize this model of pancreatitis were not altered by any of the agents tested. In contrast, both allopurinol and dimethylsulfoxide reduced peripancreatic edema formation, suggesting that edema, but not the other features that characterize this model of pancreatitis, may result from generation of oxygen-derived free radicals.

Acute Disease↗
PubMed1996

Continuing the search for cholinergic factors in cognitive dysfunction.

The objective of the experiments reported here was to explore three hypotheses regarding cholinergic processes underlying the development of progressive degenerative dementia (PDD). One possibility involved the downregulation of muscarinic receptors (mAChR) with aging, thus reducing the capability of the cholinergic system to support normal memory and other cognitive functions. The results of downregulation to 10% of normal produced only a temporary effect, the system having the capability to repair the damage. A second hypothesis predicted that a chronic hypocholinergic state can produce structural changes that are reflected in persisting cognitive dysfunctions. Chronic administration of a false cholinergic transmitter in the diets of weanling rats mimicked such a state which, if maintained for a protracted period, produced many of the features of PDD in humans. When the diet was returned to normal, biochemical and physiological processes recovered fully. However, memory impairment continued. This suggested the possibility that the behavioral losses were mediated by persisting morphological changes in the CNS. The third hypothesis proposes that these changes may be due to cell loss resulting from impaired phospholipid metabolism. Changes in sphingomyelin, one of the two major Ch-containing lipids in cell membranes, could increase amounts of ceramide, an inducer of programmed cell death (apoptosis). Tests of this hypothesis are nearing completion.

Animals↗
PubMed1992

Incomplete reversibility of an experimentally induced hypocholinergic state: biochemical and physiological, but not behavioral, recovery.

In previous reports, we described the experimental development of a hypocholinergic state in rats following the total replacement of dietary choline by an artificial isostere, N-aminodeanol (NADe). NADe shares most of the physicochemical and biochemical characteristics of choline (Ch) but is utilized less efficiently in pathways leading to the formation of both acetylcholine and phospholipids. This experimental model mimics many of the features of human degenrative dementias. We now discuss the behavioral and physiological effects of restoring a normal diet after the hypocholinergic state has become well established. The procedure by which that state was induced has been described in detail in earlier publications. After replacing Ch in the diets of weanling rats for 270 days, NADe replaced 70-85% of the phospholipid-bound Ch in plasma, brain, and peripheral tissue. When dietary NADe was removed and Ch was restored in the diet, NADe disappeared and plasma and erythrocyte (RBC) choline levels returned to normal within 30-60 days. Quinuclidinyl benzilate (QNB) binding showed that muscarinic receptors continued to be depressed in animals remaining on the NADe diet, but returned to control levels in the reversal group. There were no differences in cholinesterase activity among the three treatments. Choline acetyltransferase activity returned to control levels, while continuing to be lower in the NADe animals. Liver lipids were elevated in the latter and not significantly different in the control and reversal groups. Among physiological functions, body weight increased more rapidly in the reversal group than in animals continuing on the NADe diet. Brain weights of the reversal animals were significantly greater than those of animals not reversed, but less than controls. Core body temperatures did not differ from controls at any time during the reversal period. Behaviorally, nociceptive thresholds indicative of sensory-reflexive and sensory-perceptual responses remained significantly below normal, that is, a hyperalgesic state. Reversal animals also remained hyperactive and displayed memory significantly poorer than those on the normal diet, that is, no improvement over animals continuing on NADe. In general, the results suggest that behavioral losses induced by NADe reflect persisting changes in the CNS, despite essentially complete recovery of biochemical parameters. The changes may be morphological or be associated with adaptive changes in other neurochemical events in the CNS.

Animals↗
PubMed1984

Effect of in vivo changes in phospholipid composition on liver microsomal calcium transport.

We recently reported that the phospholipid composition of mouse liver microsomes could be altered in vivo by a combination of dietary choline deprivation and administration of the methylation inhibitors periodate-oxidized adenosine and cycloleucine (D.M. Boyle & W.L. Dean (1982) Biochim. Biophys. Acta 688, 667-670). We have now determined the effect of this in vivo change in phospholipid composition on 7 microsomal enzyme activities and 2 cytochromes. The specific contents of cytochromes b5 and P-450 were unaffected by the treatment. Similarly, NADH-cytochrome c reductase, cytochrome P-450 reductase, cyclohexane hydroxylase and Mg2+-ATPase were not significantly altered. In addition, the phospholipid/protein ratio was not changed. In contrast, Ca2+-ATPase and Ca2+ transport rates were reduced by more than 60%. This result suggests that the mouse liver microsomal Ca2+-ATPase is extremely sensitive to the phospholipid composition of the membrane in which it is embedded and that one mode of control of calcium metabolism in liver cells could be at the level of membrane phospholipid composition.

Animals↗
PubMed1990

No measurable increase in thymidine glycol or 8-hydroxydeoxyguanosine in liver DNA of rats treated with nafenopin or choline-devoid low-methionine diet.

Male rats were treated for 2 months with 1000 ppm nafenopin in the diet or for 4 or 7 days with a choline-devoid low-methionine diet. DNA was isolated from the livers and analyzed for the presence of cis-thymidine glycol-3'-phosphate (cis-dTGp) by 32P-postlabeling and for the level of 8-hydroxy-deoxyguanosine (8-OH-dG) by electrochemical detection (ECD). In no DNA sample was the level of cis-dTGp above the limit of detection of 1 modified thymidine per 10(6) nucleotides. With 8-OH-dG, a background level of this modification of 20 8-OH-dG per 10(6) nucleosides was found in liver DNA of control rats, which was not affected by either treatment. It is postulated for thymidine glycol that a potential increase was below the limit of detection or was rapidly repaired in vivo and that the steady-state level of endogenous 8-hydroxydeoxyguanosine appears not to be influenced by the treatments chosen.

8-Hydroxy-2'-Deoxyguanosine↗
PubMedDate not supplied

Effects of varying the fat content of a choline-devoid diet on promotion of the emergence of gamma-glutamyl-transpeptidase positive foci in the liver carcinogen-treated rats.

Previous studies have shown that feeding a choline-devoid (CD) diet to rats is an effective promoter of liver carcinogenesis. In the present studies, we investigated the effects of CD diets containing different levels of fat (high, 15%; low, 4%) on the induction of foci of gamma-glutamyltranspeptidase (GGT) positive hepatocytes in the liver of rats initiated with a single dose of diethylnitrosamine. In rats fed the high-fat CD diet for 4--6 weeks, a greater number of foci was induced than in rats fed similarly the low-fat CD diet. However, liver DNA synthesis and the rate of hepatocyte mitosis were not significantly different in rats fed the 2 CD diets, but were significantly higher than in rats fed a choline-supplemented diet. These results indicate that beside stimulation of liver cell proliferation, other factor(s) determine the efficacy with which a CD diet exerts its promoting action.

Animals↗
PubMed1988

Glutathione and enzymes related to free radical metabolism in liver of rats fed a choline-devoid low-methionine diet.

Fischer F-344 male rats, fed a choline-devoid diet that leads to a highly reproducible sequence of biochemical and biological changes with an ultimate development of hepatocellular carcinoma, show elevated levels of glutathione in the liver at 3, 6 and 8 days. Several enzymes related to the metabolism of free radicals, including superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase and DT-diaphorase show neither increased nor decreased activity as measured between 12 h and 8 days on the diet. Thus, of several known cellular components related to the possible scavenger of free radicals in the liver, only glutathione responded to the feeding of the CD diet. It is tentatively concluded that a decrease in the levels of possible scavengers for free radicals is not a major basis for the nuclear and mitochondrial lipid peroxidation seen early in rats fed a choline-devoid diet.

Animals↗