Protective effect of folic acid against oxidative stress produced in 21-day postpartum rats by maternal-ethanol chronic consumption during pregnancy and lactation period

2001 ◽  
Vol 34 (1) ◽  
pp. 1-8 ◽  
Author(s):  
M.J. Cano ◽  
A. Ayala ◽  
M.L. Murillo ◽  
O. Carreras
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Protective Effect ◽  
Lactation Period ◽  
Pregnancy And Lactation

scholarly journals PROTECTIVE EFFECT OF FOLIC ACID ON OXIDATIVE STRESS INDUCED BY METHIONINE OVERLOAD IN MALE MICE

2021 ◽  
Vol 21 (Suppliment-1) ◽  
pp. 1430-1434
Author(s):  
Tuqa Sabbar Rahi ◽  
Wifaq j. albazi ◽  
Ali K. Aljarah ◽  
Alaa Hussein AL-Safy
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Protective Effect ◽  
Male Mice

The Protective Effect of Cilostazol in Genotoxicity Induced by Methotrexate in Human Cultured Lymphocytes

2020 ◽  
Vol 13 (2) ◽  
pp. 137-143
Author(s):  
Abeer M. Rababa’h ◽  
Samah A. Hussein ◽  
Omar F. Khabour ◽  
Karem H. Alzoubi
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Protective Effect ◽  
Mitotic Index ◽  
Chromosomal Damage ◽  
Proliferative Index ◽  
Proliferative Effect ◽  
Phosphodiesterase Iii Inhibitor ◽  
Phosphodiesterase Iii ◽  
Healthy Body

Background: Methotrexate is an antagonist of folic acid that has been shown to be genotoxic to healthy body cells via induction of oxidative stress. Cilostazol is a phosphodiesterase III inhibitor and a potent antioxidant drug. Objectives: To evaluate the potential protective effect of cilostazol on methotrexate genotoxicity. Results: Methotrexate significantly increased the frequency of CAs and SCEs (p < 0.0001) as compared to control cultures. This chromosomal damage induced by methotrexate was considerably decreased by pretreatment of the cells with cilostazol (P < 0.01). Moreover, the results showed that methotrexate resulted in a notable reduction (P < 0.01) in cells kinetic parameters, the mitotic index (MI) and the proliferative index (PI). Similarly, cilostazol significantly reduced the mitotic index, which could be related to the anti-proliferative effect (P < 0.01). Conclusion: Methotrexate is genotoxic, and cilostazol could prevent the methotrexate-induced chromosomal damage with no modulation of methotrexate-induced cytotoxicity.

scholarly journals Whether AICAR in Pregnancy or Lactation Prevents Hypertension Programmed by High Saturated Fat Diet: A Pilot Study

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 448 ◽  
Author(s):  
Wan-Long Tsai ◽  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Saturated Fat ◽  
Nutrient Sensing ◽  
Male Offspring ◽  
Lactation Period ◽  
Sprague Dawley ◽  
Male Adult ◽  
Ampk Signaling ◽  
Pregnancy And Lactation ◽  
In Pregnancy

High consumption of saturated fats links to the development of hypertension. AMP-activated protein kinase (AMPK), a nutrient-sensing signal, is involved in the pathogenesis of hypertension. We examined whether early intervention with a direct AMPK activator 5-aminoimidazole-4-carboxamide riboside (AICAR) during pregnancy or lactation can protect adult male offspring against hypertension programmed by high saturated fat consumption via regulation of nutrient sensing signals, nitric oxide (NO) pathway, and oxidative stress. Pregnant Sprague–Dawley rats received regular chow or high saturated fat diet (HFD) throughout pregnancy and lactation. AICAR treatment was introduced by intraperitoneal injection at 50 mg/kg twice a day for 3 weeks throughout the pregnancy period (AICAR/P) or lactation period (AICAR/L). Male offspring (n = 7–8/group) were assigned to five groups: control, HFD, AICAR/P, HFD + AICAR/L, and HFD + AICAR/P. Male offspring were killed at 16 weeks of age. HFD caused hypertension and obesity in male adult offspring, which could be prevented by AICAR therapy used either during pregnancy or lactation. As a result, we demonstrated that HFD downregulated AMPK/SIRT1/PGC-1α pathway in offspring kidneys. In contrast, AICAR therapy in pregnancy and, to a greater extent, in lactation activated AMPK signaling pathway. The beneficial effects of AICAR therapy in pregnancy is related to restoration of NO pathway. While AICAR uses in pregnancy and lactation both diminished oxidative stress induced by HFD. Our results highlighted that pharmacological AMPK activation might be a promising strategy to prevent hypertension programmed by excessive consumption of high-fat food.

The role of folic acid and selenium against oxidative damage from ethanol in early life programming: a review

2018 ◽  
Vol 96 (2) ◽  
pp. 178-188 ◽  
Author(s):  
Luisa Ojeda ◽  
Fátima Nogales ◽  
Luisa Murillo ◽  
Olimpia Carreras
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Ethanol Metabolism ◽  
Postnatal Exposure ◽  
Fetal Alcohol ◽  
Early Life Programming ◽  
Dietary Antioxidant ◽  
Pregnancy And Lactation ◽  
Endogenous Antioxidants ◽  
Ethanol Ethanol

There are disorders in children, covered by the umbrella term “fetal alcohol spectrum disorder” (FASD), that occur as result of alcohol consumption during pregnancy and lactation. They appear, at least in part, to be related to the oxidative stress generated by ethanol. Ethanol metabolism generates reactive oxygen species and depletes the antioxidant molecule glutathione (GSH), leading to oxidative stress and lipid and protein damage, which are related to growth retardation and neurotoxicity, thereby increasing the incidence of FASD. Furthermore, prenatal and postnatal exposure to ethanol in dams, as well as increasing oxidation in offspring, causes malnutrition of several micronutrients such as the antioxidant folic acid and selenium (Se), affecting their metabolism and bodily distribution. Although abstinence from alcohol is the only way to prevent FASD, it is possible to reduce its harmful effects with a maternal dietary antioxidant therapy. In this review, folic acid and Se have been chosen to be analyzed as antioxidant intervention systems related to FASD because, like ethanol, they act on the methionine metabolic cycle, being related to the endogenous antioxidants GSH and glutathione peroxidase. Moreover, several birth defects are related to poor folate and Se status.

scholarly journals Synergistic protective effect of folic acid and vitamin B12against nicotine-induced oxidative stress and apoptosis in pancreatic islets of the rat

2015 ◽  
Vol 54 (3) ◽  
pp. 433-444 ◽  
Author(s):  
Ankita Bhattacharjee ◽  
Shilpi K. Prasad ◽  
Swagata Pal ◽  
Bithin Maji ◽  
Alak K. Syamal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Protective Effect ◽  
Pancreatic Islets

Antioxidant Activity and Protective Effect against Oxidative Stress on Hippocampal HT22 Cells of Tea Seed Oil

2018 ◽  
Vol 24 (1) ◽  
pp. 53-59
Author(s):  
Jong Min Kim ◽  
Seon Kyeong Park ◽  
Jin Yong Kang ◽  
Seong-kyeong Bae ◽  
Ga-Hee Jeong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Protective Effect ◽  
Seed Oil ◽  
Ht22 Cells ◽  
Tea Seed Oil

Protective effect of DJ-1 against oxidative stress: an advance

2012 ◽  
Vol 32 (1) ◽  
pp. 88-91
Author(s):  
Zhi-yong WANG ◽  
Ling-zhen TANG ◽  
Tian-wen GAO
Keyword(s):  
Oxidative Stress ◽  
Protective Effect

Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Protective Effect ◽  
Infarct Size ◽  
Rat Model ◽  
Left Ventricular ◽  
Related Factor ◽  
Nuclear Factor ◽  
Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

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