Serum Levels of Ascorbic Acid in Chronic Alcoholic Patients (with and Without Liver Damage) Attending De-Addiction Centre

Background/Aim. Patients suffered from chronic alcoholic disease very often have depression and cardiomyopathy. Treatment with several antidepressants is associated with prolonged QT interval, ventricular arrhythmias and sudden death. The aim of this study was to investigate the relation between the severity of depression, serum levels of gamma-glutamyl transferase (GGT), as a marker of liver damage, and the possible influence of paroxetine use on duration of QT interval in patient who started treatment of chronic alcoholic dependence. Methods. The study included 147 male patients (older than 18 years of age) suffering from alcohol addiction, who were also diagnosed with depressive disorder on the basis of DSM-IV criterion and positive Hamilton Rating Scale for Depression (HRSD) at the beginning of hospitalization. Out of total number of patients, 49 were randomly selected to be treated with antidepressant paroxetine at a dose of 20 mg once daily during 20 days. The global QTc interval was automatically determined. Results. By applying the generalised linear model, the statistically significant positive correlation between the length of QTc interval and serum values of GGT, that is, intensity of alcoholism (p = 0.002) and values of the HRSD score, that is, intensity of depression (p = 0.021) was established in the sample of 147 depressed alcoholic patients before the application of paroxetine. In spite of the vulnerability of patients due to the heart damage and the liver dysfunction arising from alcohol consumption, as well as altered patients' drugs metabolism, no elongation of QTc interval resulting from the application of paroxetine was established. The length of QTc interval 20 days after paroxetine administration was 401.43 ms and before paroxetine administration it was 403.31 ms. The difference in QTc interval length (after and before paroxetine administration) was ?QTc = - 1.88 ms (p = 0.524). Conclusion. The results indicated that the severity of depression and GGT serum levels positively correlated with the length of QT interval. On the other hand, paroxetine after 20 days of usage did not prolong QT interval.

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Can granulocyte colony stimulating factor (G-CSF) ameliorate acetaminophen-induced hepatotoxicity?

Human & Experimental Toxicology ◽

10.1177/09603271211008522 ◽

2021 ◽

pp. 096032712110085

Author(s):

EA Ahmed ◽

AM Abd-Eldayem ◽

E Ahmed

Keyword(s):

Liver Damage ◽

Liver Toxicity ◽

Serum Levels ◽

Hepatic Tissue ◽

Granulocyte Colony Stimulating Factor ◽

Colony Stimulating Factor ◽

Oxidative Markers ◽

Stimulating Factor ◽

New Strategies ◽

Factor G

Acetaminophen (APAP) is often used as an antipyretic and analgesic agent. Overdose hepatotoxicity, which often results in liver cell failure and liver transplantation, is a severe complication of APAP usage. To save the liver and save lives from acute liver damage caused by APAP, the search for new strategies for liver defense is important. Wistar rats have been used for the induction of APAP hepatotoxicity. Elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were evaluated for liver toxicity. In addition, the levels of hepatic tissue oxidative markers such as malondialdehyde (MDA), nitric oxide (NO) increased while glutathione (GSH) was depleted and catalase (CAT) activity was curtailed. The biochemical findings were consistent with the changes in histology that suggested liver damage and inflammation. Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high. After administration of APAP, treatment with N-AC or G-CSF substantially reduced the level of MDA and NO while maintaining the GSH content and CAT activity. Treatment with N-AC and G-CSF after administration of APAP has also attenuated inflammation and hepatocytes necrosis. The results of this study showed that G-CSF could be viewed as an alternative hepatoprotective agent against APAP-induced acute liver injury compared to N-AC.

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Serum Levels of Glutamate-Pyruvate Transaminase, Glutamate-Oxaloacetate Transaminase and Gamma-Glutamyl Transferase in 1494 Patients with Various Genotypes for the Alpha-1 Antitrypsin Gene

Journal of Clinical Medicine ◽

10.3390/jcm9123923 ◽

2020 ◽

Vol 9 (12) ◽

pp. 3923

Author(s):

José María Hernández Pérez ◽

Ignacio Blanco ◽

Agustín Jesús Sánchez Medina ◽

Laura Díaz Hernández ◽

José Antonio Pérez Pérez

Keyword(s):

Liver Damage ◽

Serum Levels ◽

Gamma Glutamyl Transferase ◽

Glutamate Oxaloacetate Transaminase ◽

Glutamate Pyruvate Transaminase ◽

Gamma Glutamyl ◽

Glutamate Pyruvate ◽

Alpha 1 Antitrypsin ◽

Glutamyl Transferase ◽

Normal Genotype

Background: Patients with liver disease associated with alpha-1 antitrypsin deficiency (AATD) are homozygous for the Z mutation, leading to chronic liver damage. Objective: To assess the serum levels of glutamate-oxaloacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), and gamma-glutamyl transpeptidase (GGT) in patients with different genotypes for the alpha-1 antitrypsin (AAT) gene. Methods: Patients (n = 1494) underwent genotyping of the SERPINA1 gene, together with a determination of AAT and GOT and GPT and GGT transaminase levels. Patients with a deficient allele (n = 476) and with a normal genotype were compared. Results: A statistically significant association was found between deficient genotypes and GOT (p < 0.0003), GPT (p < 0.002), and GGT (p < 0.006). Comparing GOT levels in patients with PI*Z deficient variant versus those with normal genotype, an odds ratio (OR) of 2.72 (CI: 1.5–4.87) (p < 0.0005) was obtained. This finding was replicated with the PI*Z allele and the GPT values (OR = 2.31; CI: 1.45–3.67; p < 0.0003). In addition, a statistically significant association was found between liver enzymes and AAT values. Conclusion: The PI*Z allele seemed to be a risk factor for the development of liver damage. AAT deficient genotypes were associated with GOT, GPT, and GGT altered values. Low AAT levels were associated with high GPT and GGT levels.

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Is Liver Enzyme Release Really Associated with Cell Necrosis Induced by Oxidant Stress?

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/3529149 ◽

2016 ◽

Vol 2016 ◽

pp. 1-12 ◽

Cited By ~ 43

Author(s):

Martha Lucinda Contreras-Zentella ◽

Rolando Hernández-Muñoz

Keyword(s):

Liver Enzyme ◽

Liver Damage ◽

Oxidant Stress ◽

Serum Levels ◽

Mitochondrial Enzymes ◽

Enzyme Release ◽

Diagnostic Features ◽

Chronic Liver Damage ◽

Hepatic Diseases

Hepatic diseases are a major concern worldwide. Increased specific plasma enzyme activities are considered diagnostic features for liver diseases, since enzymes are released into the blood compartment following the deterioration of the organ. Release of liver mitochondrial enzymes is considered strong evidence for hepatic necrosis, which is associated with an increased production of ROS, often leading to greater hepatic lipid peroxidation. Lipotoxic mediators and intracellular signals activated Kupffer cells, which provides evidence strongly suggesting the participation of oxidant stress in acute liver damage, inducing the progression of liver injury to chronic liver damage. Elevated transaminase activities are considered as an index marker of hepatotoxicity, linked to oxidant stress. However, a drastic increase of serum activities of liver enzyme markers ought not necessarily to reflect liver cell death. In fact, increased serum levels of cytoplasmic enzymes have readily been observed after partial hepatectomy (PH) in the regenerating liver of rats. In this regard, we are now showing thatin vitromodifications of the oxidant status affect differentially the release of liver enzymes, indicating that this release is a strictly controlled event and not directly related to the onset of oxidant stress of the liver.

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THE EFFECT OF REPEATED ALCOHOLIC INTOXICATION ON ADRENAL ASCORBIC ACID AND CHOLESTEROL IN THE RAT

Canadian Journal of Biochemistry and Physiology ◽

10.1139/o62-109 ◽

1962 ◽

Vol 40 (8) ◽

pp. 975-981 ◽

Cited By ~ 6

Author(s):

H. Kalant ◽

Caroline Czaja

Keyword(s):

Ascorbic Acid ◽

Relative Weight ◽

Ascorbic Acid Content ◽

Female Rats ◽

Male Rats ◽

Albino Rats ◽

Chronic Alcoholic ◽

Alcoholic Intoxication ◽

Chronic Alcoholic Intoxication ◽

Inclined Plane Test

Groups of adult male and female albino rats received daily gavage of 1.25 ml of water or of 20% ethanol per 100 g body weight for a period of 1 month, and were killed either 1.5 hours or 24 hours after the last dose. Such daily treatment with either water or alcohol, ending 24 hours before death, did not result in any significant change from control values in the relative weight of the adrenal glands, or their ascorbic acid and cholesterol contents. No changes in these values were found in animals which received an additional dose of water or alcohol 1.5 hours before death. The female rats showed lower values for adrenal ascorbic acid content than the males in corresponding groups, but did not differ from the males with respect to the effects of the various treatments. A similar experiment with male rats only, carried on for 2 months, also showed no significant differences among any of the treatment groups.Measurements of the degree of intoxication produced by single doses of ethanol were carried out by means of the inclined-plane test. Intraperitoneal injection of 2 g/kg produced much more rapid and marked intoxication than did gavage with either 2 or 4 g/kg.It was concluded that daily gavage for 1-2 months with ethanol in a moderately intoxicating dose (2 g/kg) does not constitute a stimulus to adrenal cortical activity or result in exhaustion atrophy of the adrenal cortex, and that adrenal cortical stimulation is not an invariable accompaniment of acute or chronic alcoholic intoxication.

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Comparative studies on the hypercholesterolaemia induced by excess dietary tyrosine or polychlorinated biphenyls in rats

British Journal Of Nutrition ◽

10.1079/bjn19860130 ◽

1986 ◽

Vol 56 (2) ◽

pp. 509-517 ◽

Cited By ~ 6

Author(s):

Sahoshi Nagaoka ◽

Mitsuhiro Kato ◽

Yoritaka Aoyama ◽

Akira Yoshida†

Keyword(s):

Ascorbic Acid ◽

Polychlorinated Biphenyls ◽

Comparative Studies ◽

Wistar Rats ◽

Serum Levels ◽

Liver Lipids ◽

Male Wistar Rats

1. The effects of dietary polychlorinated biphenyls (PCB) and excess tyrosine on serum and liver lipids, urinary ascorbic acid and catecholamines were compared in male Wistar rats.2. Serum levels of cholesterol, urinary ascorbic acid, norepinephrine, epinephrine, dopamine and histamine were significantly increased in rats given either PCB or excess tyrosine.3. The hypercholesterolaemia induced by PCB or excess tyrosine was blocked by the adrenergic α-blocker, phenoxybenzamine.4. The present results suggest causal interrelations between the hypercholesterolaemia induced by dietary PCB or excess tyrosine and the secretion of catecholamines.

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Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection

Current Issues in Molecular Biology ◽

10.3390/cimb43030139 ◽

2021 ◽

Vol 43 (3) ◽

pp. 2022-2035

Author(s):

Manuela G. Neuman ◽

Lawrence B. Cohen

Keyword(s):

Cell Death ◽

Chronic Hepatitis ◽

Hepatitis C ◽

Viral Infection ◽

Liver Damage ◽

Inflammatory Markers ◽

Pathogenic Bacteria ◽

Serum Levels ◽

Control Group ◽

Inflammatory Status

Hepatitis C virus (HCV)-induced liver disease contributes to chronic hepatitis. The immune factors identified in HCV include changes in the innate and adaptive immune system. The inflammatory mediators, known as “inflammasome”, are a consequence of the metabolic products of cells and commensal or pathogenic bacteria and viruses. The only effective strategy to prevent disease progression is eradication of the viral infection. Immune cells play a pivotal role during liver inflammation, triggering fibrogenesis. The present paper discusses the potential role of markers in cell death and the inflammatory cascade leading to the severity of liver damage. We aim to present the clinical parameters and laboratory data in a cohort of 88 HCV-infected non-cirrhotic and 25 HCV cirrhotic patients, to determine the characteristic light microscopic (LM) and transmission electron microscopic (TEM) changes in their liver biopsies and to present the link between the severity of liver damage and the serum levels of cytokines and caspases. A matched HCV non-infected cohort was used for the comparison of serum inflammatory markers. We compared the inflammation in HCV individuals with a control group of 280 healthy individuals. We correlated the changes in inflammatory markers in different stages of the disease and the histology. We concluded that the serum levels of cytokine, chemokine, and cleaved caspase markers reveal the inflammatory status in HCV. Based upon the information provided by the changes in biomarkers the clinician can monitor the severity of HCV-induced liver damage. New oral well-tolerated treatment regimens for chronic hepatitis C patients can achieve cure rates of over 90%. Therefore, using the noninvasive biomarkers to monitor the evolution of the liver damage is an effective personalized medicine procedure to establish the severity of liver injury and its repair.

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Phytochemical Screening and Hepatoprotective Potential of Aqueous Fruit Pulp Extract of Adansonia digitata against CCL4 Induced Liver Damage in Rats

Asian Journal of Biochemistry, Genetics and Molecular Biology ◽

10.9734/ajbgmb/2020/v3i330086 ◽

2020 ◽

pp. 12-21

Author(s):

A. M. Sa’id ◽

A. H. Musa ◽

J. A. Mashi ◽

F. U. Maigari ◽

M. N. Nuhu

Keyword(s):

Aqueous Extract ◽

Liver Damage ◽

Serum Levels ◽

Health Science ◽

Fruit Pulp ◽

Medical Sciences ◽

Adansonia Digitata ◽

Hepatoprotective Effects ◽

Dose Dependent ◽

Basic Medical

Aim: The current study was carried out to evaluate the hepatoprotective effects of aqueous extract of Adansonia digitata fruit pulp on carbon tetrachloride (CCl4) induced liver damage in rats. Place and Duration of Study: Department of Biochemistry, Faculty of Basic Medical Sciences, College of Health Science, between November 2017 and January 2018. Methodology: A. digitata fruit pulp was extracted by maceration using water; and a concentration of 100 mg/ml was used. Two doses of the aqueous extract (200 mg/kg and 300 mg/kg) and Livoline (25 mg/kg) were used to investigate their hepatoprotective effects on CCl4-induced hepatotoxicity in rats. Results: The two doses of the plant extract showed dose-dependent hepatoprotective effect on CCl4-induced hepatotoxicity, as evident by the significant reduction (P<0.05) in serum levels of AST, ALT, ALP and bilirubin along with the improved histopathological liver sections compared to CCl4-treated animals. Conclusion: Due to its hepatoprotective potentials, A. digitata extract may be used to develop standard treatment drugs against some liver disorders when it is further evaluated through extensive researches.

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Influence of methyl and isopropyl N-methyl antranilates on carbon tetrachloride-induced changes in rat liver morphology and function

Facta universitatis - series Physics Chemistry and Technology ◽

10.2298/fupct1301067r ◽

2013 ◽

Vol 11 (1) ◽

pp. 67-73 ◽

Cited By ~ 10

Author(s):

Niko Radulovic ◽

Pavle Randjelovic ◽

Nikola Stojanovic ◽

Ivan Ilic ◽

Ana Miltojevic

Keyword(s):

Carbon Tetrachloride ◽

Liver Damage ◽

Serum Levels ◽

Protective Effects ◽

Liver Lesions ◽

Human Diet ◽

Histopathological Evaluation ◽

Liver Morphology ◽

And Function ◽

Induced Changes

The aim of the present study was to examine potential protective effects of methyl N-methylanthranilate (M) and isopropyl N-methylanthranilate (I) in a rat model of acute intoxication with carbon tetrachloride (CCl4) by tracking the changes in liver morphology and function. Serum transaminase and bilirubin were significantly elevated in animals treated with CCl4 alone. A pretreatment with M and I prior to the administration of CCl4 significantly prevented the increase of serum levels of liver damage markers. Histopathological evaluation of the livers of the test animals also revealed that M and I reduced the incidence of liver lesions. Our experiments showed that both M and I possess protective effect in CCl4-induced liver damage in rats. The results are of interest due to the presence of natural or synthetic M in the human diet.

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Hepatoprotective Actions of Ascorbic Acid, Alpha Lipoic Acid and Silymarin or Their Combination Against Acetaminophen-Induced Hepatotoxicity in Rats

Medicina ◽

10.3390/medicina55050181 ◽

2019 ◽

Vol 55 (5) ◽

pp. 181 ◽

Cited By ~ 2

Author(s):

Anmar M. Abdulrazzaq ◽

Mujtaba Badr ◽

Omar Gammoh ◽

Asad A. Abu Khalil ◽

Bayan Y. Ghanim ◽

...

Keyword(s):

Oxidative Stress ◽

Ascorbic Acid ◽

Liver Function ◽

Lipoic Acid ◽

Rat Hepatocytes ◽

Serum Levels ◽

Liver Function Tests ◽

Alpha Lipoic Acid

Background and objectives: Ascorbic acid, alpha lipoic acid (ALA) and silymarin are well-known antioxidants that have hepatoprotective effects. This study aims to investigate the effects of these three compounds combined with attenuating drug-induced oxidative stress and cellular damage, taking acetaminophen (APAP)-induced toxicity in rats as a model both in vivo and in vitro. Materials and Methods: Freshly cultured primary rat hepatocytes were treated with ascorbic acid, ALA, silymarin and their combination, both with and without the addition of APAP to evaluate their in vitro impact on cell proliferation and mitochondrial activity. In vivo study was performed on rats supplemented with the test compounds or their combination for one week followed by two toxic doses of APAP. Results: Selected liver function tests and oxidative stress markers including superoxide dismutase (SOD), malondialdehyde (MDA) and oxidized glutathione (GSSG) were detected. The in vivo results showed that all three pretreatment compounds and their combination prevented elevation of SOD and GSSG serum levels indicating a diminished burden of oxidative stress. Moreover, ascorbic acid, ALA and silymarin in combination reduced serum levels of liver enzymes; however, silymarin markedly maintained levels of all parameters to normal ranges. Silymarin either alone or combined with ascorbic acid and ALA protected cultured rat hepatocytes and increased cellular metabolic activity. The subjected agents were capable of significantly inhibiting the presence of oxidative stress induced by APAP toxicity and the best result for protection was seen with the use of silymarin. Conclusions: The measured liver function tests may suggest an augmented hepatoprotection of the combination preparation than when compared individually.

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