The modulation of lipid peroxidation by the folic acid during liver regeneration

1994 ◽  
Vol 21 ◽  
pp. S155
Keyword(s):  
Lipid Peroxidation ◽  
Folic Acid ◽  
Liver Regeneration

ENHANCERS OF LIVER REGENERATION IN ONCOLOGICAL SURGERY

2021 ◽  
Vol 108 (Supplement_3) ◽  
Author(s):  
M Osorio Capitan ◽  
S Rose ◽  
I Novo Sukia ◽  
B Herrero de la Parte ◽  
I Ruiz Montesinos ◽  
...  
Keyword(s):  
Folic Acid ◽  
Liver Function ◽  
Liver Regeneration ◽  
Control Group ◽  
Depressant Effect ◽  
Oncological Surgery ◽  
Portal Branch ◽  
Treatment Control ◽  
Early Application ◽  
Mean Size

Abstract INTRODUCTION Chemotherapy hinders liver function and probably its regenerating capacity, forcing to delay it after surgery. Our objective has been to verify this effect in an experimental model and to see if a hepatotrophic agent can prevent it. MATERIAL AND METHODS Four groups of 6 WAG/RijHsd rats (males, 3-4 months) were submitted to ligation of the portal branch to the left lateral and left paramedian lobes. They were sacrificed 36 h later to quantify the percentage of liver corresponding to the ligated lobes (weight), the number of hepatocyte’s nuclei (nº/100 µm2) and their mean size (µm2). One group received no treatment (control); another folic acid (2.5 mg/kg ip, during surgery); other 5-Fluorouracil (5-FU 50 mg/kg ip 48 h before); and the fourth received folic&5-FU. RESULTS The animals treated with folic acid showed a greater number of hepatocyte’s nuclei (24.4 ± 2.77 vs 15.2 ± 1.51) and their mean size was also greater (121 ± 2.34 vs 111 ± 1.8). However, the reduction in weight of the ligated parenchyma was less than in control group (33.4 ± 1.08 vs 29.5 ± 1.08). 5-FU did not modify the number of nuclei (15.6 ± 18.4), although they were smaller in size (104 ± 1.7). The addition of folic acid to 5-FU increased the number of nuclei (21.7 ± 2.8) and normalized their size (111 ± 3.2). CONCLUSIONS 5-FU exerts a depressant effect on livers regeneration, and folic acid overcomes it. Thus, folic acid could allow early application of chemotherapy without affecting liver regeneration.

scholarly journals Modulation of Balance Between Apoptosis and Proliferation by Lipid Peroxidation (LPO) During Rat Liver Regeneration

2002 ◽  
Vol 8 (12) ◽  
pp. 808-817 ◽  
Author(s):  
María Teresa Ronco ◽  
María de Luján Alvarez ◽  
Juan Monti ◽  
María Cristina Carrillo ◽  
Gerardo Pisani ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Liver Regeneration ◽  
Rat Liver ◽  
Rat Liver Regeneration

Oxidative stress and platelet activation in subjects with moderate hyperhomocysteinaemia due to MTHFR 677 C→T polymorphism

2012 ◽  
Vol 108 (09) ◽  
pp. 533-542 ◽  
Author(s):  
Alfredo Dragani ◽  
Angela Falco ◽  
Francesca Santilli ◽  
Stefania Basili ◽  
Giancarlo Rolandi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Folic Acid ◽  
Platelet Activation ◽  
Methylenetetrahydrofolate Reductase ◽  
Folic Acid Supplementation ◽  
Control Group ◽  
Loading Test ◽  
Study Objective ◽  
Acid Supplementation

SummaryThe methylenetetrahydrofolate reductase (MTHFR) 677 C→T polymorphism may be associated with elevated total homocysteine (tHcy) levels, an independent risk factor for cardiovascular disease. It was the study objective to evaluate in vivo lipid peroxidation and platelet activation in carriers of the MTHFR 677 C→T polymorphism and in non-carriers, in relation to tHcy and folate levels. A cross-sectional comparison of urinary 8-iso-prostaglandin (PG)F2α and 11-dehydro-thromboxane (TX)B2 (markers of in vivo lipid peroxidation and platelet activation, respectively) was performed in 100 carriers and 100 non-carriers of the polymorphism. A methionine-loading test and folic acid supplementation were performed to investigate the causal relationship of the observed associations. Urinary 8-iso-PGF2α and 11-dehydro-TXB2 were higher in carriers with hyperhomocysteinaemia than in those without hyperhomocysteinaemia (p<0.0001). Hyperhomocysteinaemic carriers had lower folate levels (p=0.0006), higher urinary 8-iso-PGF2α (p<0.0001) and 11-dehydro-TXB2 (p<0.0001) than hyperhomocysteinaemic non-carriers. On multiple regression analysis, high tHcy (p<0.0001), low folate (p<0.04) and MTHFR 677 C→T polymorphism (p<0.001) independently predicted high rates of 8-iso-PGF2α excretion. Methionine loading increased plasma tHcy (p=0.002), and both urinary prostanoid metabolites (p=0.002). Folic acid supplementation was associated with decreased urinary 8-iso-PGF2α and 11-dehydro-TXB2 excretion (p<0.0003) in the hyperhomocysteinaemic group, but not in the control group, with substantial inter-individual variability related to baseline tHcy level and the extent of its reduction. In conclusion, hyperhomocysteinaemia due to the MTHFR 677 C→T polymorphism is associated with enhanced in vivo lipid peroxidation and platelet activation that are reversible, at least in part, following folic acid supplementation. An integrated biomarker approach may help identifying appropriate candidates for effective folate supplementation.

scholarly journals Changes in dietary folate intake differentially affect oxidised lipid and mitochondrial DNA damage in various brain regions of rats in the absence/presence of intracerebroventricularly injected amyloid β-peptide challenge

2011 ◽  
Vol 105 (9) ◽  
pp. 1294-1302 ◽  
Author(s):  
Ta-Fu Chen ◽  
Ming-Jang Chiu ◽  
Chou-Tz Huang ◽  
Ming-Chi Tang ◽  
Sue-Jane Wang ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Dna Damage ◽  
Folic Acid ◽  
Neuronal Death ◽  
Brain Regions ◽  
Folate Intake ◽  
Amyloid Β Peptide ◽  
Aβ Peptide ◽  
Dietary Folate ◽  
Dietary Folate Intake

Accumulating evidence suggests that changes in dietary folate intake may modulate the risks of Alzheimer's disease (AD) through as yet unknown mechanisms. The aims of the present study were to investigate how dietary folate affects the brain folate distribution, levels of oxidised lipid and DNA damage in the absence/presence of β-amyloid(25–35)(Aβ) peptide challenge, a pathogenic hallmark of AD. Male Wistar rats were assigned to diets with folic acid at 0 (folate deprivation; FD), 8 (moderate folate; MF) and 8 mg folic acid/kg diet+0·003 % in drinking-water (folate supplementation; FS) for 4 weeks. A single injection of Aβ peptide (1 mg/ml) or the vehicle solution was intracerebroventricularly (icv) administrated to rats a week before killing. Brain folate, a marker of oxidative injury, and neuronal death were assayed. In the absence of an Aβ injection, FD rats showed reduced folate levels, and increased 2-thiobarbituric acid-reactive substances and a mitochondrial (mt)DNA 4834 bp large deletion (mtDNA4834deletion) in the hippocampus compared with the counterpart brains of control rats (P < 0·05). A single icv injection of Aβ peptide potentiated lipid peroxidation in the medulla of FD rats, which was ameliorated by feeding FD rats with the MF and FS diets (P < 0·05). Feeding the FS diet to Aβ-injected rats enriched brain folate levels and reduced mtDNA4834deletion in the hippocampal and medullary regions compared with corresponding tissues of Aβ+FD rats (P < 0·05). Aβ+FS rats had reduced rates of neuronal death in the frontal cortex compared with Aβ+FD rats (P < 0·05). Taken together, our data revealed that folate deprivation differentially depleted brain folate levels, and increased lipid peroxidation and mtDNA4834deletions, particularly, in the hippocampus. Upon Aβ challenge, the FS diet may protect various brain regions against lipid peroxidation, mitochondrial genotoxicity and neural death associated with folate deprivation.

scholarly journals Acute ethanol preexposure promotes liver regeneration after partial hepatectomy in mice by activating ALDH2

2014 ◽  
Vol 306 (1) ◽  
pp. G37-G47 ◽  
Author(s):  
Xiang Ding ◽  
Juliane I. Beier ◽  
Keegan J. Baldauf ◽  
Jenny D. Jokinen ◽  
Hai Zhong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Lipid Peroxides ◽  
Ethanol Exposure ◽  
Mitochondrial Enzyme ◽  
Aldehyde Dehydrogenase 2 ◽  
Acute Ethanol ◽  
Cell Cycle Regulatory Genes

It is known that chronic ethanol significantly impairs liver regeneration. However, the effect of acute ethanol exposure on liver regeneration remains largely unknown. To address this question, C57Bl6/J mice were exposed to acute ethanol (6 g/kg intragastrically) for 3 days, and partial hepatectomy (PHx) was performed 24 h after the last dose. Surprisingly, acute ethanol preexposure promoted liver regeneration. This effect of ethanol did not correlate with changes in expression of cell cycle regulatory genes (e.g., cyclin D1, p21, and p27) but did correlate with protection against the effect of PHx on indices of impaired lipid and carbohydrate metabolism. Ethanol preexposure protected against inhibition of the oxidant-sensitive mitochondrial enzyme, aconitase. The activity of aldehyde dehydrogenase 2 (ALDH2) was significantly increased by ethanol preexposure. The effect of ethanol was blocked by inhibiting (Daidzin) and was mimicked by activating (Alda-1) ALDH2. Lipid peroxides are also substrates for ALDH2; indeed, alcohol preexposure blunted the increase in lipid peroxidation (4OH-nonenal adducts) caused by PHx. Taken together, these data suggest that acute preoperative ethanol exposure “preconditions” the liver to respond more rapidly to regenerate after PHx by activating mitochondrial ALDH2, which prevents oxidative stress in this compartment.

scholarly journals Effect of vitamin C on liver regeneration after partial hepatectomy and acetaminophen-induced liver injury in Wistar rats

2021 ◽  
Vol 8 (2) ◽  
pp. 489
Author(s):  
Reno Rudiman ◽  
Handy Wing ◽  
Nurhayat Usman
Keyword(s):  
Lipid Peroxidation ◽  
Liver Injury ◽  
Vitamin C ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Wistar Rats ◽  
Liver Weight ◽  
Potential Effect ◽  
Regeneration Rate ◽  
Male Wistar Rats

Background: The aim of this study is to evaluate the potential effect of vitamin C as an antioxidant on liver regeneration after partial hepatectomy and acetaminophen-induced liver injury in Wistar rats.Methods: A total of 24 male Wistar rats were divided into four groups, each group consisted of 6 rats: group A (control, partial hepatectomy/PHx alone), group B (PHx and vitamin C 250 mg/kg BW), group C (acetaminophen 500 mg/kg BW and PHx), and group D (acetaminophen 500 mg/kg BW with PHx and vitamin C 250 mg/kg BW). Subtoxic dose of acetaminophen was given 24 hours before partial hepatectomy. Vitamin C was given orally via oral gavage for 6 consecutive days after partial hepatectomy. POD 7, all animals were terminated and performed laparotomy to obtain liver tissue for measurement of liver weight and regeneration rate, blood samples for malondialdehyde (MDA) as a lipid peroxidation measurement and histopathological investigation.Results: The means of regeneration rate in vitamin C groups were significantly higher compared to non-vitamin C group (p<0.05). Similar result, the means of MDA values in vitamin C groups were significantly lower compared to non-vitamin C group (p<0.05). This result suggests a protective effect of vitamin C against lipid peroxidation. Histopathological changes in liver cells were statistically difference between vitamin C groups and non-vitamin C groups (p<0.05).Conclusions: Our results indicate that vitamin C administration promotes liver regeneration and inhibits lipid peroxidation after partial hepatectomy and acetaminophen-induced liver injury in Wistar rats.

Bevacizumab Allows Preservation of Liver Function and its Regenerative Capacity after Major Hepatectomy

2019 ◽  
Vol 19 (11) ◽  
pp. 1388-1398
Author(s):  
Amparo Valverde ◽  
Rubén Ciria ◽  
Javier Caballero-Villarraso ◽  
Patricia Aguilar-Melero ◽  
Gustavo Ferrín ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Liver Regeneration ◽  
Major Hepatectomy ◽  
High Dose ◽  
Histopathological Analysis ◽  
Liver Resections ◽  
Tnf Α ◽  
Toxicity Analysis ◽  
The Impact

Background: Parallel to the safety of liver resections, new chemotherapy drugs have emerged for the control of liver metastases. However, there is unclear evidence about the combination of intensive BVZ-therapy and extended resections. The main aim was to analyse the impact of Bevacizumab (BVZ) in terms of liver safety and tolerability in two experimental models: a basal-toxicity situation and after major hepatectomy. Methods: Eighty male-Wistar rats were grouped as toxicity analysis (sham-operated rats-OS-) and regenerationafter- surgery analysis (hepatectomy rats-H-). Eight further subgroups were created according to sacrifice (6- hours-6h- or 24-hours-24h-) and dose (μg) of BVZ (none, 100, 200, 400). Several measurements were performed, including biochemical serum samples, histopathological analysis, cytokines (IL-6, TNF-α, TGF-β), oxidative-stress (GSH/GSSG, ATP), lipid-peroxidation (TBARS) and epidermal and vascular endothelium growth-factors (EGF and VEGF). Results: In the toxicity analysis, safe results with BVZ were observed, with no significant differences among the groups. A trend towards a lower oxidative status was observed in the OS 6 h-100, -200 and -400 versus the OS 6 h-none group. Similar results were observed in the hepatectomy model, with stable oxidative-stress-index and IL-6, TNF- α, and TGF- β levels. Despite higher lipid peroxidation status, overall regeneration was preserved. As expected, VEGF was almost undetectable in BVZ-treated groups after resection, but not in the non-resection group. Conclusion: It was concluded that liver status was not impaired by BVZ even at the high-dose. Similarly, liver regeneration after extended hepatectomy in BVZ-treated animals was well-preserved. Extended liver resections may be encouraged in BVZ-treated patients due to its excellent tolerability and good liver regeneration status.

Folic acid supplemented goat milk has beneficial effects on hepatic physiology, haematological status and antioxidant defence during chronic Fe repletion

2014 ◽  
Vol 82 (1) ◽  
pp. 86-94 ◽  
Author(s):  
María JM Alférez ◽  
Emilio Rivas ◽  
Javier Díaz-Castro ◽  
Silvia Hijano ◽  
Teresa Nestares ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Folic Acid ◽  
Goat Milk ◽  
Cow Milk ◽  
Control Group ◽  
Antioxidant Defence ◽  
Folate Supplementation ◽  
Dietary Folate ◽  
Enzymatic Antioxidant ◽  
Beneficial Effects

The aim of the current study was to asses the effect of goat or cow milk-based diets, either normal or Fe-overloaded and folic acid supplement on some aspects of hepatic physiology, enzymatic antioxidant defence and lipid peroxidation in liver, brain and erythrocyte of control and anaemic rats after chronic Fe repletion. 160 male Wistar rats were placed on 40 d in two groups, a control group receiving normal-Fe diet and the Fe-deficient group receiving low Fe diet. Lately, the rats were fed with goat and cow milk-based diets during 30 d, with normal-Fe content or Fe-overload and either with normal folic or folic acid supplemented. Fe-overload increased plasma alanine transaminase and aspartate transaminase levels when cow milk was supplied. Dietary folate supplementation reduced plasma transaminases levels in animals fed goat milk with chronic Fe overload. A remarkable increase in the superoxide dismutase activity was observed in the animals fed cow milk. Dietary folate supplement lead to a decrease on the activity of this enzyme in all the tissues studied with both milk-based diets. A concomitant increment in catalase was also observed. The increase in lipid peroxidation products levels in rats fed cow milk with Fe-overload, suggest an imbalance in the functioning of the enzymatic antioxidant defence. In conclusion, dietary folate-supplemented goat milk reduces both plasma transaminases levels, suggesting a hepatoprotective effect and has beneficial effects in situation of Fe-overload, improving the antioxidant enzymes activities and reducing lipid peroxidation.

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