scholarly journals Melatonin Inhibits Benzene-Induced Lipid Peroxidation in Rat Liver

2010 ◽  
Vol 61 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Seema Sharma ◽  
Suresh Rana
Keyword(s):  
Lipid Peroxidation ◽  
Single Dose ◽  
Rat Liver ◽  
Treated Group ◽  
Melatonin Treatment ◽  
Liver Histopathology ◽  
Microsomal Lipid Peroxidation ◽  
Significant Difference ◽  
Mitochondrial Lipid

Melatonin Inhibits Benzene-Induced Lipid Peroxidation in Rat LiverWe studied the antioxidative role of melatonin against benzene toxicity in rat liver. The inhibition of mitochondrial and microsomal lipid peroxidation differed between 24-hour (single-dose), 15-day, and 30-day treatments. Inhibition of mitochondrial lipid peroxidation was the highest after the single dose of melatonin, whereas highest microsomal inhibition was recorded after 30 days of melatonin treatment. No significant difference was recorded between 15-day and 30-day treatments. Cytochrome P 4502E1 (CYP 4502E1) activity declined after the single-dose and 15-day melatonin treatment in the benzene-treated group, but it rose again, though not significantly after 30 days of treatment. Liver histopathology generally supported these findings. Phenol concentration in the urine samples declined in melatonin and benzene-treated rats. Our results show that melatonin affects CYP 4502E1, which is responsible for benzene metabolism. Inhibition of its metabolism correlated with lower lipid peroxidation. In conclusion, melatonin was found to be protective against lipid peroxidation induced by benzene.

Antimalarial Drugs Exacerbate Rat Liver Microsomal Lipid Peroxidation in the Presence of Oxidants

2001 ◽  
Vol 21 (3) ◽  
pp. 353-359 ◽  
Author(s):  
E. Olatunde Farombi ◽  
Stanley Adoro ◽  
Samuel Uhunmwangho
Keyword(s):  
Lipid Peroxidation ◽  
Rat Liver ◽  
Lipid Hydroperoxide ◽  
Antimalarial Drugs ◽  
Oxygen Species ◽  
Radical Chain ◽  
Microsomal Lipid Peroxidation ◽  
Hydroperoxide Formation ◽  
Chain Breaking

The study was undertaken to evaluate the effect of prior treatment of rats with the antimalarial drugs amodiaquine (AQ) mefloquine (MQ) and halofantrine (HF) on rat liver microsomal lipid peroxidation in the presence of 1 mM FeSO4, 1 mM ascorbate and 0.2 mM H2O2 (oxidants). Ingestion of α-tocopheral, a radical chain-breaking antioxidant was also included to assess the role of antioxidants in the drug treatment. In the presence of oxidants AQ, MQ and HF elicited 288%, 175% and 225% increases in malondialdehyde (MDA) formation while the drugs induced 125%, 63% and 31% increases in the absence of oxidants respectively. Similarly, AQ, MQ and HF induced lipid hydroperoxide formation by 380%, 256%, 360% respectively in the presence of oxidants and 172%, 136% and 92% in the absence of exogenously added oxidants respectively. α-tocopherol reduced AQ, MQ and HF-induced MDA formation by 40%, 55% and 52% respectively and lipid hydroperoxide formation by 53%, 59% and 54% respectively. Similarly, α-tocopherol attenuated the AQ, MQ and HF-induced MDA formation by 49%, 51% and 51% in the presence of oxidants and lipid hydroperoxide formation by 61%, 62% and 47% respectively. The results indicate that rat liver microsomal lipid peroxidation could be enhanced by antimalarial drugs in the presence of reactive oxygen species and this effect could be ameliorated by treatment with antioxidants.

The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat erythrocytes: role of vitamins E and C

2007 ◽  
Vol 23 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Recep Sutcu ◽  
Irfan Altuntas ◽  
Bora Buyukvanli ◽  
Onur Akturk ◽  
Ozlem Ozturk ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Single Dose ◽  
Treated Group ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Organophosphate Insecticide ◽  
Rat Erythrocytes ◽  
Vitamins E And C

Reactive oxygen species caused by organophosphates may be involved in the toxicity of various pesticides. Therefore, in this study, we aimed to investigate the effects of acute exposure to organophosphate insecticide diazinon (DI) and possible ameliorating role of vitamins E and C, with the following parameters: lipid peroxidation (LPO) and the activity of the glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in rat erythrocytes. The experimental groups were arranged as control group, DI-treated group (DI) and DI + vitamin E + vitamin C—treated group (DI + Vit). DI + Vit groups were treated orally with a single dose of 335 mg/kg DI body weight. Vitamins E and C were injected at doses of 150 mg/kg body weight intramuscular (in) and 200 mg/kg body weight intraperitoneal (ip), respectively, 30 min after the treatment of DI in DI + Vit group. Blood samples were taken 24 h after the DI. The results showed that DI administration caused to increase in LPO and the activities of SOD and GSH-Px enzymes in erythrocytes. Also, the combination of vitamins E and C decreased LPO and the activities of GSH-Px and SOD compared with the DI group. In conclusion, although treating rats with single dose DI increases LPO and antioxidant enzyme activities in erythrocytes, vitamins C and E combination can reduce LPO caused by DI. Toxicology and Industrial Health 2007; 23: 13—17.

Microsomal lipid peroxidation and oxidative metabolism in rat liver: Influence of vitamin A intake

1984 ◽  
Vol 50 (3) ◽  
pp. 361-366 ◽  
Author(s):  
W.M. Tom ◽  
L.Y.Y. Fong ◽  
D.Y.H. Woo ◽  
Vitoon Prasongwatana ◽  
T.R.C. Boyde
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin A ◽  
Rat Liver ◽  
Oxidative Metabolism ◽  
Microsomal Lipid Peroxidation

The Contribution of Sex Difference on Different Liver Histopathology Between Male and Female Mice After Oral Administration of Caffeine

2021 ◽  
Vol 2 (2) ◽  
pp. 37-41
Author(s):  
Muhammad Sholikhuddin Nafi’ ◽  
Tri Hartini Yuliawati ◽  
Prijati Sri Irawati ◽  
Nurina Hasanatuludhhiyah
Keyword(s):  
Oral Administration ◽  
Sex Difference ◽  
Liver Cell ◽  
Histopathological Examination ◽  
Treated Group ◽  
Male And Female ◽  
Female Mice ◽  
Liver Histopathology ◽  
End Of Treatment ◽  
Significant Difference

Background : There are several studies reporting the effect of caffeine on liver histopathology, but it remains controversy. The laboratory animal used in those studies were predominantly male, whereas there is contribution of sex difference on different liver reaction to xenobiotic between male and female subject. Objective : It is necessary to conduct a study to explore the differences between the liver histopathology of male and female mice after oral administration of caffeine. Methods : This study used 36 mice (Mus musculus) that were divided into 4 groups: male & female untreated groups and male & female treated groups which were orally administered with caffeine 0.4 mg / 20 gramBW daily for 30 days. At the end of treatment, mice were euthanized and dissected. Histopathological examination was done to determine the percentage of  liver cell death of each group. Results: The percentage of liver cell deathin female treated group was higher than male treated group (p = 0.0001). But there was no significant difference of liver cells death between male control and treated group and between female control and treated group. Conclusion : There was significant difference in liver histopathology between male and female mice after oral administration of caffeine.

Abstract 450: The Role of CD38 as a Therapeutic Target for Protection Against Doxorubicin-induced Cardiotoxicity Through Nad+ Boosting

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Thais R Peclat ◽  
Guillermo Agorrody ◽  
Lilian S Gomez ◽  
Eduardo N Chini
Keyword(s):  
Single Dose ◽  
Therapeutic Target ◽  
Potential Role ◽  
Damage Mechanism ◽  
Treated Group ◽  
Wild Type ◽  
Chemotherapeutic Treatment ◽  
Positive Effect ◽  
Dose Injection

Background: Doxorubicin is a chemotherapy medication used to treat several types of cancer. Its major adverse effect is cardiotoxicity, which may limit its use. Doxorubicin-induced cardiotoxicity (DIC), once developed, carries a poor prognosis. Therefore strategies to prevent or treat DIC are of paramount importance but have not yet been fully developed. Being NAD + a critical nucleotide which is involved in oxy-reduction reactions and CD38 the main NAD + -consuming enzyme responsible for NAD levels regulation and homeostasis, we aim to investigate the link of CD38 and NAD + metabolism in DIC and its potential role as a therapeutic target. Methods: We compared Wild-type (WT) control mice with WT mice treated with a single dose injection of 15 mg/kg of doxorubicin who received vehicle or an antibody that blocksCD38 ecto-enzymatic activity. We also compared genetically CD38 catalytic inactive (CI) mice treated or not with the same single dose injection. Results: Doxorubicin caused a decrease in Ejection Fraction (EF) in WT mice. We also observed that CD38 CI mice treated with doxorubicin did not have changes in EF compared to their control. When compared to WT receiving just doxorubicin, WT mice treated also with the antibody had a trend to improve EF. As for exercise performance, our results show a decrease in exercise capacity induced by doxorubicin that was reversed in the antibody group and did not happen in the CD38 CI mice treated with doxorubicin. Doxorubicin caused a decrease in heart rate variability (HRV) which was improved in the antibody treated group. Moreover, our results show a survival rate that is similar to what has been previously shown, with 50% mortality associated with doxorubicin. Blockage of CD38 activity with antibody reduced mortality in this model to approximately 20%. Mechanistically, we did not observe decreases in NAD+ levels induced by Doxorubicin. However, boost of NAD induced by blocking CD38 was related to protection against DIC. Conclusion: Our results indicate that the damage mechanism of DIC may not be related directly with NAD decrease, but NAD boosting induced by CD38 blockage seems to have a positive effect in protection against cardiac dysfunction related to this chemotherapeutic treatment.

The effects of organophosphate insecticide methidathion on lipid peroxidation and anti-oxidant enzymes in rat erythrocytes: role of vitamins E and C

2002 ◽  
Vol 21 (12) ◽  
pp. 681-685 ◽  
Author(s):  
I Altuntas ◽  
N Delibas ◽  
R Sutcu
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Single Dose ◽  
Treated Group ◽  
Control Group ◽  
Organophosphate Insecticide ◽  
Rat Erythrocytes ◽  
Vitamins E And C ◽  
Anti Oxidant ◽  
C 30

The effects of organophosphate insecticide methidathion (MD) on lipid peroxidation and anti-oxidant enzymes and the ameliorating effects of a combination of vitamins E and C against MD toxicity were evaluated in rat erythrocytes. Experimental groups were: control group, MD-treated group (MD), and MD+vitamin E+vitamin Ctreated group (MD+Vit). MD and MD+Vit groups were treated orally with a single dose of 8 mg/kg MD body weight at 0 hour. Vitamins E and C were injected at doses of 150 mg/kg body weight, i.m. and 200 mg/kg body weight, i.p., respectively, 30 min after the treatment of MD in the MD+Vit group. Blood samples were taken 24 hours after the MD administration. The level of malondialdehyde (MDA), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were studied in the erythrocytes. MDA level increased significantly in the MD group compared to the control group (P <0.05) and decreased significantly in the MD+Vit group compared to the MD group (P <0.05). The activities of SOD, GSH-Px, and CAT decreased in the MD group compared to the control group (P<0.05). Only GSH-Px activity increased in the MD+Vit group compared with the MD group. These results suggest that treating rats with MD increases LPO and decreases anti-oxidant enzyme activities in erythrocytes. Furthermore, single-dose treatment with a combination of vitamins E and C 30 min after the administration of MD can reduce LPO caused by MD.

scholarly journals Effect of NADPH on the Microsomal Lipid Peroxidation in the Presence of the Soluble Fraction of Rat Liver

1978 ◽  
Vol 98 (6) ◽  
pp. 757-763 ◽  
Author(s):  
MASAKI SATO ◽  
YUZO AMIKURA ◽  
TACHIO AIMOTO ◽  
RYOHEI KIMURA ◽  
TOSHIRO MURATA
Keyword(s):  
Lipid Peroxidation ◽  
Rat Liver ◽  
Soluble Fraction ◽  
Microsomal Lipid Peroxidation
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