scholarly journals Defensive role of silibinin against arsenic induced oxidative stress mediated dyslipidemia and neurotoxicity in rats

2016 ◽  
Vol 4 (1) ◽  
pp. 78 ◽  
Author(s):  
Muthumani Muthu ◽  
Sumedha Naroem Chanu ◽  
Shagirtha Kalist ◽  
Milton Prabu
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Properties ◽  
Brain Regions ◽  
Lipid Profiles ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Ros Production ◽  
Protein Carbonyl Content ◽  
Defensive Role ◽  
The Brain

Arsenic (As) is an environmental toxic metalloid that is present in everywhere such as air, water and soil. Generally, inorganic arsenic has a tendency to be more toxic than organic arsenic. The present study was designed to determine whether oral administration of silibinin (SB), which has been shown to have substantial antioxidant properties, when pre-administered (75 mg/kg body weight) once daily for 4 weeks along with arsenic (5 mg/kg) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX),glutathione-S-transferase (GST),glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione (GSH), total sulfhydryl groups (TSH) and vitamin C in rat brain regions such as cortex, striatum, cerebellum, hippocampus and brain stem. Our study also examined the effect of SB over arsenic-induced reactive oxygen species (ROS) production and lipid peroxidation level (LPO) and protein carbonyl content (PC) in distinct brain regions of rats. Moreover, As also alters the lipid profiles such as total lipids, phospholipids, cholesterol, cerebrosides and gangliosides in various regions of the brain. Pre-administration of SB restores the altered enzymatic and non-enzymatic antioxidants, lipid profiles and also markedly reduced the ROS, LPO, PC and accumulation of As in various regions of the brain. These results suggested that arsenic-induced deficits in antioxidant enzyme activities and increase in ROS production and lipid peroxidation levels in brain regions can be remarkably prevented by pre-administration of SB. 

scholarly journals ROS Production Is Increased in the Kidney but Not in the Brain of Dahl Rats With Salt Hypertension Elicited in Adulthood

2015 ◽  
pp. 303-312 ◽  
Author(s):  
M. VOKURKOVÁ ◽  
H. RAUCHOVÁ ◽  
L. ŘEZÁČOVÁ ◽  
I. VANĚČKOVÁ ◽  
J. ZICHA
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Nadph Oxidase ◽  
Salt Intake ◽  
Renal Medulla ◽  
High Salt ◽  
Ros Production ◽  
High Salt Intake ◽  
Salt Hypertension ◽  
The Brain

Enhanced production of superoxide radicals by nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase in the brain and/or kidney of salt hypertensive Dahl rats has been proposed to participate in the pathogenesis of this form of experimental hypertension. Most information was obtained in young Dahl salt-sensitive (DS) rats subjected to high salt intake prior to sexual maturation. Therefore, the aim of our study was to investigate whether salt hypertension induced in adult DS rats is also accompanied with a more pronounced oxidative stress in the brain or kidney as compared to Dahl salt-resistant (DR) controls. NADPH oxidase activity as well as the content of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes (oxidative index), which indicate a degree of lipid peroxidation, were evaluated in two brain regions (containing either hypothalamic paraventricular nucleus or rostral ventrolateral medulla) as well as in renal medulla and cortex. High salt intake induced hypertension in DS rats but did not modify blood pressure in DR rats. DS and DR rats did not differ in NADPH oxidase-dependent production of ROS, TBARS content or oxidative index in either part of the brain. In addition, high-salt diet did not change significantly any of these brain parameters. In contrast, the enhanced NADPH oxidase-mediated ROS production (without significant signs of increased lipid peroxidation) was detected in the renal medulla of salt hypertensive DS rats. Our findings suggest that there are no signs of enhanced oxidative stress in the brain of adult Dahl rats with salt hypertension induced in adulthood.

scholarly journals New Insights on Hemp Oil Enriched in Cannabidiol: Decarboxylation, Antioxidant Properties and In Vitro Anticancer Effect

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 738
Author(s):  
Anca Roxana Petrovici ◽  
Natalia Simionescu ◽  
Andreea Isabela Sandu ◽  
Vasile Paraschiv ◽  
Mihaela Silion ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cancer Cells ◽  
Antioxidant Properties ◽  
Flash Chromatography ◽  
Ros Production ◽  
Antioxidant Power ◽  
Anticancer Effects ◽  
Induced Apoptosis ◽  
Hemp Oil

This study aimed to obtain and characterize extracted hemp oil enriched in cannabidiol (CBD) by decarboxylation of cannabidiolic acid (CBDA) and to give new insights into its antioxidant and anticancer effects. Optimization of CBDA decarboxylation in hemp oil was performed, and CBD and CBDA contents and purities were determined by flash chromatography, 1H- and 13C-NMR. The antioxidant properties of CBD-enriched oil were investigated by Fe2+ chelating activity, Fe3+ reducing antioxidant power assay, O2− scavenging activity, HO− scavenging ability and lipid peroxidation inhibitory assay, and its cytotoxicity, apoptosis- and oxidative stress-inducing effects on NHDF, MeWo, HeLa, HepG2 and HOS cells were determined. The CBD concentration in hemp oil was increased by CBDA soft decarboxylation optimized at 90 °C, for 1 h and the resulting oil was capable of reducing iron, scavenging free radicals and inhibiting lipid peroxidation in cell-free oxidative conditions. CBD-enriched oil promoted NHDF proliferation at up to 15 µg CBD/mL, while inducing apoptosis and ROS production and modulating antioxidant enzymes’ gene expression in cancer cells, being selective for osteosarcoma cells, and induced apoptosis by p53- and ROS-independent mechanisms. CBD-enriched hemp oil demonstrated antioxidant properties in oxidative conditions and promoted normal fibroblasts’ proliferation, while inducing apoptosis and ROS production in cancer cells.

scholarly journals Diphenyl diselenide and diphenyl ditelluride increase the latency for 4-aminopyridine-induced chemical seizure and prevent death in mice.

2009 ◽  
Vol 56 (1) ◽  
Author(s):  
Verônica B Brito ◽  
João Batista T Rocha ◽  
Vanderlei Folmer ◽  
Fernando Erthal
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Properties ◽  
Neuroprotective Activity ◽  
Dependent Manner ◽  
Significant Incidence ◽  
Diphenyl Ditelluride ◽  
Clonic Seizures ◽  
Pre Treatment ◽  
Dose Dependent ◽  
The Brain

In this work was investigated the effect of pre-treatment with (PhSe)(2) and (PhTe)(2) on chemical seizure and 4-aminopyridine-induced lethality in mice. Additionally, lipid peroxidation levels of whole brain after treatment with 4-aminopyridine and effect of pre-treatment with (PhSe)(2) and (PhTe)(2) on these levels were investigated. Mice were pre-treated with (PhSe)(2) or (PhTe)(2) (50, 100, or 150 micromol/kg) 30 min before 4-aminopyridine (12 mg/kg) administration. The treatment with 4-aminopyridine caused a significant incidence of seizures (clonic, tonic) and death. Pre-treatment with (PhSe)(2) and (PhTe)(2) significantly increased the latency for clonic and tonic seizures, and prevented 4-aminopyridine-induced death. Significantly, the pre-treatment with (PhSe)(2) or (PhTe)(2) increased the latency for clonic seizures in a dose-dependent manner. Additionally, a significant increase was observed in the brain lipid peroxidation level after treatment with 4-aminopyridine, which was significantly inhibited by pre-treatment with 150 micromol/kg (PhSe)(2) or (PhTe)(2). These results demonstrate that (PhSe)(2) and (PhTe)(2) counteract the harmful effects of 4-aminopyridine. It is possible that this effect results from modulation of the redox state of N-methyl-d-aspartate receptors and/or of Ca(2+) channel activity with subsequent alteration in neurotransmitter release. Importantly, this study provides evidence for anticonvulsant and antioxidant properties of (PhSe)(2) and (PhTe)(2), which indicates a neuroprotective activity of these compounds.

scholarly journals New Insights on Hemp Oil Enriched in Cannabidiol: Decarboxylation, Antioxidant Properties and In Vitro Anticancer Effect

2021 ◽  
Author(s):  
Anca Roxana Petrovici ◽  
Natalia Simionescu ◽  
Andreea Isabela Sandu ◽  
Vasile Paraschiv ◽  
Mihaela Silion ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cancer Cells ◽  
Antioxidant Properties ◽  
Flash Chromatography ◽  
Ros Production ◽  
Antioxidant Power ◽  
Anticancer Effects ◽  
Induced Apoptosis ◽  
Hemp Oil

This study aimed to obtain and characterize extracted hemp oil enriched in cannabidiol (CBD) by decarboxylation of cannabidiolic acid (CBDA) and to give new insights into its antioxidant and anticancer effects. Optimization of CBDA decarboxylation in hemp oil was performed, and CBD and CBDA contents and purities were determined by “flash chromatography”, 1H- and 13C-NMR. The antioxidant properties of CBD-enriched oil were investigated by Fe2+ chelating activity, Fe3+ reducing antioxidant power assay, O2− scavenging activity, HO− scavenging ability and lipid peroxidation inhibitory assay and its cytotoxicity, apoptosis- and oxidative stress-inducing effects on NHDF, MeWo, HeLa, HepG2 and HOS cells were determined. The CBD concentration in hemp oil was increased by CBDA soft decarboxylation optimized at 90°C, for 1 h and resulted oil was capable of reducing iron, scavenging free radicals, and inhibiting lipid peroxidation in cell-free oxidative conditions. CBD-enriched oil promoted NHDF proliferation at up to 15 µg CBD/mL, while inducing apoptosis and ROS production and modulating antioxidant enzymes’ gene expression in cancer cells, being selective for osteosarcoma cells and induced apoptosis by p53- and ROS-independent mechanisms. CBD-enriched hemp oil demonstrated antioxidant properties in oxidative conditions and promoted normal fibroblasts’ proliferation, while inducing apoptosis and ROS production in cancer cells.

scholarly journals Investigation into the effects of antioxidant-rich extract ofTamarindus indicaleaf on antioxidant enzyme activities, oxidative stress and gene expression profiles in HepG2 cells

PeerJ ◽  
2015 ◽  
Vol 3 ◽  
pp. e1292 ◽  
Author(s):  
Nurhanani Razali ◽  
Azlina Abdul Aziz ◽  
Chor Yin Lim ◽  
Sarni Mat Junit
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Leaf Extract ◽  
Cholesterol Biosynthesis ◽  
Xenobiotic Metabolism ◽  
Coagulation System ◽  
Antioxidant Enzyme Activities ◽  
Ros Production ◽  
Immune Protection

The leaf extract ofTamarindus indicaL. (T. indica) had been reported to possess high phenolic content and showed high antioxidant activities. In this study, the effects of the antioxidant-rich leaf extract of theT. indicaon lipid peroxidation, antioxidant enzyme activities, H2O2-induced ROS production and gene expression patterns were investigated in liver HepG2 cells. Lipid peroxidation and ROS production were inhibited and the activity of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase was enhanced when the cells were treated with the antioxidant-rich leaf extract. cDNA microarray analysis revealed that 207 genes were significantly regulated by at least 1.5-fold (p< 0.05) in cells treated with the antioxidant-rich leaf extract. The expression ofKNG1, SERPINC1, SERPIND1, SERPINE1, FGG, FGA, MVK, DHCR24, CYP24A1,ALDH6A1, EPHX1andLEAP2were amongst the highly regulated. When the significantly regulated genes were analyzed using Ingenuity Pathway Analysis software, “Lipid Metabolism, Small Molecule Biochemistry, Hematological Disease” was the top biological network affected by the leaf extract, with a score of 36. The top predicted canonical pathway affected by the leaf extract was the coagulation system (P< 2.80 × 10−6) followed by the superpathway of cholesterol biosynthesis (P< 2.17 × 10−4), intrinsic prothrombin pathway (P< 2.92 × 10−4), Immune Protection/Antimicrobial Response (P< 2.28 × 10−3) and xenobiotic metabolism signaling (P< 2.41 × 10−3). The antioxidant-rich leaf extract ofT. indicaalso altered the expression of proteins that are involved in the Coagulation System and the Intrinsic Prothrombin Activation Pathway (KNG1, SERPINE1, FGG), Superpathway of Cholesterol Biosynthesis (MVK), Immune protection/antimicrobial response (IFNGR1, LEAP2, ANXA3 and MX1) and Xenobiotic Metabolism Signaling (ALDH6A1, ADH6). In conclusion, the antioxidant-rich leaf extract ofT. indicainhibited lipid peroxidation and ROS production, enhanced antioxidant enzyme activities and significantly regulated the expression of genes and proteins involved with consequential impact on the coagulation system, cholesterol biosynthesis, xenobiotic metabolism signaling and antimicrobial response.

Antioxidant Properties of Solenostemma argel Effervescent Tablets

2019 ◽  
Vol 20 (8) ◽  
pp. 679-688
Author(s):  
Rasha S. Suliman ◽  
Heyam S. Ali ◽  
Khulud Alhelal ◽  
Wejdan Almutairi ◽  
Shahd Alnasser ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Methanolic Extract ◽  
Antioxidant Activities ◽  
Histopathological Examination ◽  
Antioxidant Properties ◽  
Butylated Hydroxytoluene ◽  
Antioxidant Enzyme Activities ◽  
Super Oxide Dismutase ◽  
Function Test ◽  
Mice Liver

Objective: In the present study, Solenostemma argel effervescent tablets were prepared from Argel methanolic extract. Methods: The tablets were examined for their ability to impede carbon tetrachloride (CCl4)-induced lipid peroxidation in mice liver. The antioxidant activities of the enzymes; super-oxide dismutase (SOD), glutathione peroxidase (GS-PX) along with malondialdehyde level were tested in liver tissues. Results: The obtained results indicated that the antioxidant enzyme activities were remarkably reduced while the level of Malondialdehyde (MDA), which shows lipid peroxidation, and the activity of alanine aminotransferase (a liver function test) were remarkably intensified following intra-peritoneal i.p injection with the single sub-lethal hepatotoxic dose of CCl4 compared to the control. A necrotic lesion in the liver of mice injected with CCl4 was observed by the histopathological examination. The damaging influence of CCl4 was improved by the retreatment with Argel or BHT, which could also be observed in the normal appearance of the liver tissue. Conclusion: In this study, it was concluded that S. Argel and butylated hydroxytoluene (BHT) could be effective by decreasing lipid peroxidation and increasing the activities of antioxidant enzymes. Therefore, Argel might be applied as a hepatoprotective agent without any side effects.

Protective effect of curcumin against lead neurotoxicity in rat

2003 ◽  
Vol 22 (12) ◽  
pp. 653-658 ◽  
Author(s):  
Pradeep K Shukla ◽  
Vinay K Khanna ◽  
Mohd Y Khan ◽  
Rikhab C Srimal
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Protective Effect ◽  
Corpus Striatum ◽  
Reduced Glutathione ◽  
Antioxidant Property ◽  
Brain Regions ◽  
Lead Levels ◽  
The Brain

Curcumin (diferuloylmethane), an active ingredient of turmeric, is known to have multiple activities, including an antioxidant property, and has been suggested to be of use in treatment of several diseases. The present study has been undertaken to investigate the protective effect of curcumin against lead-induced neurotoxicity in rats. Exposure of rats to lead (50 mg/kg po) for 45 days caused an increase in lipid peroxidation (LPO) and a decrease in reduced glutathione (GSH) levels in cerebellum, corpus striatum, hippocampus and frontal cortex as compared with controls. Lead levels were significantly increased in these rats. Activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) decreased in all the brain regions following lead exposure. Interestingly, cotreatment with curcumin (100 mg/kg po) and lead (50 mg/kg po) for 45 days caused a significant decrease in LPO with concomitant decrease in lead levels in all the brain regions as compared with those treated with lead alone. A significant increase in reduced glutathione (GSH) levels, SOD and CAT activities was also observed in all the four brain regions in rats simultaneously treated with curcumin and lead. The results suggest that curcumin may prevent lead-induced neurotoxicity.

Effect of selenium on vanadium toxicity in different regions of rat brain

1998 ◽  
Vol 17 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Syed Saleem Haider ◽  
A A Abdel-Gayoum ◽  
Mustafa El-Fakhri ◽  
Kilani M Ghwarsha
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Protective Effect ◽  
Rat Brain ◽  
Sulfhydryl Group ◽  
Brain Regions ◽  
Neurotoxic Effects ◽  
Selenium Treatment ◽  
Vanadium Toxicity ◽  
The Brain

The protective effect of selenium on the neurotoxicity of vanadium in different brain regions of rats was investigated. The lipid peroxidation was significantly accentuated after intraperitoneal (i.p.) administration of vanadium (1.5 mg kg71 b.wt) for a period of 12 consecutive days to rats. The increase in lipid peroxidation was inhibited by selenium treatment (0.02 mg kg71 b.wt., i.p.) for 12 consecutive days. Vanadium exposure produced a decrease in nonprotein sulfhydryl group. Selenium treatment prevented the depression in nonprotein sulfhydryl group in all the brain regions of the vanadium exposed rats. The concentration of ascorbic acid was decreased after co-administration of selenium and vanadium. These results suggest that selenium protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulfhydryl groups. The decrease in ascorbic acid levels may have been due to its consumption in forming complexes with vanadium.

scholarly journals The antioxidant role of Sideritis caesarea infusion against TCA toxicity in rats

2010 ◽  
Vol 105 (5) ◽  
pp. 663-668 ◽  
Author(s):  
Ismail Celik ◽  
Mehmet Salih Kaya
Keyword(s):  
Superoxide Dismutase ◽  
Green Tea ◽  
Antioxidant Properties ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Aerial Parts ◽  
Mda Content ◽  
Group B ◽  
The Brain

Sideritis caesarea (SC) Duman, Aytac&Baser is a member of the Lamiaceae family. The present study was designed to investigate the antioxidant properties of the aerial parts of island green tea SC against TCA effects in rats. Biomarkers selected for monitoring antioxidant capacity were the activities of glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase, catalase (CAT), GSH level and malondialdehyde (MDA) content in various organs of rats. Three experimental groups, A (untreated = control), B (only TCA-treated) and C (TCA+SC-treated), were studied. At the end of the 50 d experiment, the MDA content in tissues increased significantly in group B, whereas no significant changes were observed in group C as compared with that of the control group. Antioxidant enzyme activities such as SOD and CAT increased significantly in the brain, liver and kidneys of group B but decreased significantly in group C as compared with group B. The GSH level and GR activity increased significantly in the brain and liver of group C as compared with the control and TCA-exposed rats. Hence, the study reveals that the constituents present in SC impart protection against chemical-induced oxidative injury that may result in the development of cancer.

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