Modulation of calcium by the carcinogenic process in the liver induced by a choline-deficient diet

1987 ◽  
Vol 65 (3) ◽  
pp. 478-482 ◽  
Author(s):  
Amiya K. Ghoshal ◽  
Ezio Laconi ◽  
Frederick Willemsen ◽  
Amit Ghoshal ◽  
Thomas H. Rushmore ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Liver Cell ◽  
Cell Cancer ◽  
Deficient Diet ◽  
Triglyceride Accumulation ◽  
Dna Alterations ◽  
Preneoplastic Foci ◽  
Carcinogenic Process ◽  
Induced Changes

A diet devoid of choline and low in methionine (CD), without any added carcinogen, has been shown to induce 100% preneoplastic nodules and more than 50% cancer in the rat liver. Attempts to understand the mechanism by which a CD diet induces liver cell cancer revealed that like chemical carcinogens, a CD diet also appears to cause alterations in DNA, perhaps mediated by free radicals. Indeed, a CD diet induces nuclear lipid peroxidation prior to the changes in DNA. The CD diet induced DNA alterations coupled with continuing liver cell proliferation may account for the induction of initiated hepatocytes by the CD diet. To gain insight into the nature of free radicals generated by the CD diet, experiments were designed to determine whether agents that modulate free radical effects influence the CD diet induced changes in the liver. We investigated the effect of Ca2+ in the modulation of CD diet induced alterations in the liver. The results show that extra Ca2+ when added to the CD diet prevented some of the early changes due to choline deficiency, such as nuclear lipid peroxidation and DNA damage, but had little or no effect on the triglyceride accumulation in the liver. Also, the same CD diet with extra Ca2+, when used as a promoter after initiation by diethylnitrosamine, decreased the number and size of early putative preneoplastic foci and nodules.

Role of free radicals in catecholamine-induced cardiomyopathy

1982 ◽  
Vol 60 (11) ◽  
pp. 1390-1397 ◽  
Author(s):  
P. K. Singal ◽  
N. Kapur ◽  
K. S. Dhillon ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Free Radicals ◽  
Vitamin E ◽  
Creatine Phosphate ◽  
Normal Diet ◽  
Ultrastructural Changes ◽  
Antioxidant Vitamin ◽  
Deficient Diet ◽  
Increased Sensitivity ◽  
Increase Membrane Permeability ◽  
Induced Changes

Effects of an antioxidant, vitamin E, and a membrane stabilizing agent, zinc, were examined on the isoproterenol-induced changes in the rat myocardium. Isoproterenol treatment (80 mg/kg given over 2 days in two equal doses) caused arrhythmias and 25% mortality within 24 h of the last injection. The ultrastructural changes in the subendocardium and in focal areas of the subepicardium included swelling of mitochondria, loss of myofibrils, cell necrosis, fibrosis, and infiltration of the affected areas by polymorphonucleocytes. Both creatine phosphate and adenosine triphosphate levels were markedly decreased in hearts from isoproterenol-treated animals. Pretreatment of the animals with vitamin E (10 mg∙kg−1∙day−1 for 2 weeks) or zinc (10 mg/kg ZnSO4, twice a day for 7 days) prevented these deleterious effects of isoproterenol. Animals maintained on vitamin E deficient diet for 8 weeks were found to be more sensitive to isoproterenol-induced changes and this increased sensitivity was reversed by a 2-week feeding of the animals on the normal diet coupled with vitamin E treatment. Based on the data obtained in this study it is proposed that catecholamine-induced changes may involve free radicals, which by promoting lipid peroxidation may increase membrane permeability and lead to the development of cardiomyopathy.

Phenolic constituents and inhibitory effects of the leaf of Rauvolfia vomitoria Afzel on free radicals, cholinergic and monoaminergic enzymes in rat’s brain in vitro

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Olubukola H. Oyeniran ◽  
Adedayo O. Ademiluyi ◽  
Ganiyu Oboh
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Methanolic Extract ◽  
Array Detector ◽  
Oh Radicals ◽  
Inhibitory Effects ◽  
Methanolic Extracts ◽  
Phenolic Constituents ◽  
Rauvolfia Vomitoria

AbstractObjectivesRauvolfia vomitoria is a medicinal plant used traditionally in Africa in the management of several human diseases including psychosis. However, there is inadequate scientific information on the potency of the phenolic constituents of R. vomitoria leaf in the management of neurodegeneration. Therefore, this study characterized the phenolic constituents and investigated the effects of aqueous and methanolic extracts of R. vomitoria leaf on free radicals, Fe2+-induced lipid peroxidation, and critical enzymes linked to neurodegeneration in rat’s brain in vitro.MethodsThe polyphenols were evaluated by characterizing phenolic constituents using high-performance liquid chromatography coupled with diode array detector (HPLC-DAD). The antioxidant properties were assessed through the extracts ability to reduce Fe3+ to Fe2+; inhibit ABTS, DPPH, and OH radicals and Fe2+-induced lipid peroxidation. The effects of the extracts on AChE and MAO were also evaluated.ResultsThe phenolic characterization of R. vomitoria leaf revealed that there were more flavonoids present. Both aqueous and methanolic extracts of R. vomitoria leaf had inhibitory effects with the methanolic extract having higher significant (p≤0.05) free radicals scavenging ability coupled with inhibition of monoamine oxidases. However, there was no significant (p≤0.05) difference obtained in the inhibition of lipid peroxidation and cholinesterases.ConclusionThis study suggests that the rich phenolic constituents of R. vomitoria leaf might contribute to the observed antioxidative and neuroprotective effects. The methanolic extract was more potent than the aqueous extract; therefore, extraction of R. vomitoria leaf with methanol could offer better health-promoting effects in neurodegenerative condition.

Ethane production as a measure of lipid peroxidation after renal ischemia

1986 ◽  
Vol 251 (5) ◽  
pp. F839-F843 ◽  
Author(s):  
M. S. Paller ◽  
R. P. Hebbel
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Superoxide Radical ◽  
Oxygen Free Radicals ◽  
Tissue Injury ◽  
Renal Ischemia ◽  
Radical Scavenger ◽  
Base Line ◽  
Ethane Production

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.

scholarly journals Malondialdehyde levels can be measured in serum and saliva by using a fast HPLC method with visible detection / Determinarea printr-o metodă HPLC-VIS rapidă a concentraţiilor serice şi salivare ale malondialdehidei

2016 ◽  
Vol 24 (3) ◽  
pp. 319-326 ◽  
Author(s):  
Erzsébet Fogarasi ◽  
Mircea Dumitru Croitoru ◽  
Ibolya Fülöp ◽  
Enikő Nemes-Nagy ◽  
Robert Gabriel Tripon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Unsaturated Fatty Acids ◽  
Pearson Correlation ◽  
Living Organism ◽  
Hplc Method ◽  
Limit Of Quantification ◽  
Pearson Correlation Test ◽  
Repeated Sample

Abstract Oxidative stress appears when the amount of free radicals that are formed in a living organism exceed its spin-trapping ability. One of the most dangerous free radicals that are formed in the human body is the hydroxyl radical. It can alter several biomolecules, including the unsaturated fatty acids; this process is known as lipid peroxidation and can lead to cell necrosis and generation of several harmful byproducts including malondialdehyde, which serves also as a biomarker of oxidative stress. A new HPLC method with visible detection was developed for the detection of malondialdehyde in human serum and saliva samples. The method was verified in terms of specificity, linearity, limits of detection (0.35 ng/ml), limit of quantification (1.19 ng/ml), recovery (90.13±10.25 – 107.29±14.33) and precision (3.84±1.49% – 6.66±1.76%). An analysis time of only 1 minute was obtained and no interferences from the matrices were observed. Statistical analysis (Pearson correlation test) showed a moderate correlation (R = 0.5061, p = 0.0099) between serum and saliva concentrations (N = 25). The possibility of measuring salivary concentrations of malondialdehyde extents the applications of oxidative stress/lipid peroxidation estimations to categories of population unreachable before (pregnant women, small children, etc); repeated sample studies are also easier to make.

Manganese neurotoxicity: a model for free radical mediated neurodegeneration?

1982 ◽  
Vol 60 (11) ◽  
pp. 1398-1405 ◽  
Author(s):  
John Donaldson ◽  
Duncan McGregor ◽  
Frank LaBella
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Neuropsychiatric Symptoms ◽  
Brain Regions ◽  
Neonatal Rats ◽  
Manganese Neurotoxicity ◽  
Neuronal Homeostasis ◽  
Significant Depression ◽  
Disease Study ◽  
Bizarre Behavior

In man, manganese neurointoxication is characterised in the early phase by bizarre behavior reminiscent of that observed in schizophrenia. During chronic manganese intoxication the neuropsychiatric symptoms manifested earlier disappear and are followed by a permanent neurological phase typified by extrapyramidal symptoms similar to those of Parkinson's disease. Study of manganese intoxication in animals may provide important clues towards elucidation of the biochemical defect underlying neuropsychiatric as well as extrapyramidal diseases. Investigations in our laboratory suggest that neurotoxicity of manganese is an exaggeration of function in normal neuronal homeostasis. Manganese neurointoxication in neonatal rats resulted in significant depression of lipid peroxidation in several rat brain regions examined. In the striatum, lipid peroxidative activity was abolished, an effect which may be related to alteration in neurotransmitters often observed in the striatum of manganese-treated rats. The chronic, extrapyramidal stage of manganism, may ensue when excess Mn2+ is oxidised to higher valency forms where it can potentiate the autoxidation of catecholamines, like dopamine, resulting in concomitant formation of free radicals and cytotoxic quinones. This latter effect may arise preferentially in the substantia nigra, where neuromelanin is formed nonenzymatically by autoxidation of dopamine.

Role of Free Radicals and Lipid Peroxidation in Gastric Mucosal Injury Induced by Ischemia-Reperfusion in Rats

1989 ◽  
Vol 24 (sup162) ◽  
pp. 55-58 ◽  
Author(s):  
S. Ueda ◽  
T. Yoshikawa ◽  
S. Takahashi ◽  
H. Ichikawa ◽  
M. Yasuda ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury

Free Radicals and Lipid Peroxidation in Liver of Rats Kept on a Diet Devoid of Choline

1989 ◽  
Vol 7 (3-6) ◽  
pp. 233-240 ◽  
Author(s):  
S. Banni ◽  
F. P. Corongiu ◽  
M. A. Dessi ◽  
A. Iannone ◽  
B. Lombardi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals
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