Antioxidant properties of black tea in alcohol intoxication

Food ingredients such as alcohol may modify cellular redox state. Ethanol metabolism is accompanied by generation of free radicals that can damage cell components especially when antioxidant mechanisms are no able to neutralize them. However black tea is a source of polyphenol antioxidants that may enhance cellular antioxidant abilities. The aim of this study was to investigate the effect of black tea on antioxidant abilities of the liver, blood serum and brain of 12-months old rats sub-chronically (for 28 days) intoxicated with ethanol. Administration of black tea alone caused increase in the activity and concentration of antioxidant parameters more extensively in the liver and serum than in the brain. Alcohol caused decrease in the liver glutathione peroxidase and reductase and catalase activity but increase in activity of superoxide dismutase. Moreover, decrease in the level of non-enzymatic antioxidants, such as reduced glutathione, vitamin C, A and E and β-carotene was observed. The activity of serum glutathione peroxidase and reductase decreased while superoxide dismutase activity was not changed. The level of non-enzymatic antioxidants in serum was also decreased. However brain activity/level of all examined antioxidants enzymatic as well as non-enzymatic was decreased after ethanol intoxication. Black tea considerably prevented antioxidant parameters against changes caused by ethanol. These results indicate beneficial antioxidant effect of black tea regarding all examined tissues, but especially the liver.     

Evaluation Of The Diuretic Activity Of Boerhaavia Verticillata

The present investigation was undertaken to evaluate the potential diuretic activity of Boerhaavia verticillata . The ethanolic and aqueous extracts of B. verticillata were administered in doses of 50 and 100 mg/kg, i.p., to normal and adult albino rats, which were monitored over a period of 24 h. Experimental results confirmed that both the ethanol and aqueous extracts have diuretic properties, but the ethanol extract seems to have less diuretic and natriuretic activity than the aqueous extract.     

Luteolin promotes mitochondrial protection during acute and chronic periods of isoproterenol induced myocardial infarction in rats

ObjectiveAn attempt has been made to evaluate the mitochondrial protection in acute and chronic periods after isoproterenol (ISO)-induced myocardial-infarction (MI) in male Wistar rats.Materials and methodsLuteolin was supplemented by intra-gastric intubation at a daily dose of 0.3 mg/kg body weight for 30 days. In the acute MI model, luteolin had been administered once per day to rat groups during 30 days. On 29th and 30th days, the rats of the acute MI control groups were administered 85 mg/kg body weight, isoproterenol, intra-peritoneally at an interval of 24 h. In the chronic MI model luteolin was supplemented to the rat group during 30 days. On the 1st and 2nd days, the rats of the chronic MI control and luteolin treatment groups were administered ISO by the same way.ResultsThe isoproterenol-treated rats both in acute and chronic models showed an increase in the level of TBARS and a decrease in the activities of mitochondrial antioxidants in MI rats, an increase in levels of mitochondrial lipid profile except phospholipids and the activities of mitochondrial enzymes were decreased in isoproterenol-treated rats. Oral treatments with luteolin in both acute and chronic models showed a significant decrease in the levels of mitochondrial lipid peroxidation, increase in the mitochondrial antioxidant levels and also decrease in the mitochondrial enzymes.ConclusionThus the present study revealed that luteolin ameliorates mitochondrial damage in isoproterenol induced myocardial infarction by maintaining lipid peroxidation metabolism due to its free radical scavenging, mitochondrial lipids, antioxidants and mitochondrial enzymes. Histopathological observations were also in correlation with the biochemical parameters.     

Alcohol stress on cardiac tissue – Ameliorative effects of Thespesia populnea leaf extract

BackgroundCells are naturally equipped with antioxidant defenses to counterbalance free radical production. Overproduction of free radicals is one of the reasons for a variety of diseases. The current investigation was planned to evaluate chronic alcohol- (for 30 days) induced oxidative stress in the cardiac tissue of rat and to explore the effectiveness of Thespesia populnea (TP)-induced cardio-protection in rat heart by utilizing an in vivo model of cardiac injury by alcohol.MethodsTen groups of rats were maintained and were divided into different groups. Alcohol 20% was administered and Thespesia leaf extracts (TPE) were administered at a dose of 250 mg/kg to chronic alcoholic rats for 30 days. The heart tissue was isolated and processed for further analysis, and also blood for estimation of blood alcohol level and serum creatine phosphokinase (CPK). The activities/levels of antioxidant enzymes, malondialdehyde (MDA), and protein carbonyls (PC) were estimated using established protocols. Histopathology was performed as evidence for the work and to establish the results.ResultsActivities of antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and reduced glutathione content (GSH) showed a decrease, while glutathione-S-transferase (GST) activity, MDA, and PC recorded an elevation due to alcohol treatment in the cardiac tissue compared to the control rats. Alcohol-induced myocardial injury was observed, indicated by a significant increase in serum CPK, a well-known biomarker of myocardial injury, and histopathological evidence supported these observations by revealing predominantly extensive edema with vacuolization and severe necrosis.ConclusionTreatment with TPE confers protection on the heart tissue during alcohol-induced oxidative stress, and thereby minimizes oxidative damage to the cardiac tissue as clearly marked in histopathology.     

Anti-inflammatory effect of a fatty acid mixture with high ω-9:ω-6 ratio and low ω-6:ω-3 ratio on rats submitted to dental extraction

ObjectiveTo evaluate the anti-inflammatory effect of pretreatment for three days with a fatty acid mixture with high ω-9:ω-6 ratio and low ω-6:ω-3 ratio on rats submitted to dental extraction.Material and methodsThirty-two male Wistar rats (270–310 g) were randomly distributed in four groups (n = 8/group): the sham control group and the negative control group received saline; the high omega-6/low omega-9 group received isolipid fatty acid with high ω-6:ω-3 ratio and low ω-9:ω-6 ratio; the high omega-3/low omega-6 group received fatty acid with low ω-6:ω-3 ratio and high ω-9:ω-6 ratio. Saline and oils were administered by gavage for 4 days before exodontia and 3 days after surgery, followed by euthanasia. Masseter edema was evaluated clinically and tissue samples were submitted to osteoclast count (H&E), myeloperoxidase assay, and western blotting (tumor necrosis factor-alpha and interleukin-1beta).ResultsIn the high omega-3/low omega-6 group, a significant decrease was observed in masseter edema (p < 0.0001), myeloperoxidase (p < 0.0001), osteoclasts (p = 0.0001) and TNF-α expression (p < 0.0001), but not in IL-1β expression.ConclusionThe ingestion of fatty acid with high ω-9:ω-6 ratio and low ω-6:ω-3 ratio significantly reduced inflammatory response in rats submitted to dental extraction.     

Molecular action mechanisms of solar infrared radiation and heat on human skin

The generation of ROS underlies all solar infrared-affected therapeutic and pathological cutaneous effects. The signaling pathway NF-kB is responsible for the induced therapeutic effects, while the AP-1 for the pathological effects. The different signaling pathways of infrared-induced ROS and infrared-induced heat shock ROS were shown to act independently multiplying the influence on each other by increasing the doses of irradiation and/or increasing the temperature.The molecular action mechanisms of solar infrared radiation and heat on human skin are summarized and discussed in detail in the present paper. The critical doses are determined. Protection strategies against infrared-induced skin damage are proposed.     

ACEMg supplementation ameliorates progressive Connexin 26 hearing loss in a child

Mutations in the gene encoding Connexin 26 are the most common cause of genetic hearing loss. The hearing loss is typically stable but may be progressive. The reason for progression is unknown. Antioxidants have been associated with attenuation of hearing loss from other insults. One antioxidant regimen consists of beta-carotene (metabolized to vitamin A), vitamin C, vitamin E, and magnesium (ACEMg). We present a child with Connexin 26 related hearing loss who experienced progressive hearing loss over 7 years of observation. He was given ACEMg daily for 3 years, during which time his progressive hearing loss was ameliorated.     

Neuroprotective effects of dimerumic acid and deferricoprogen from Monascus purpureus NTU 568-fermented rice against 6-hydroxydopamine-induced oxidative stress and apoptosis in differentiated pheochromocytoma PC-12 cells

Context Oxidative stress plays a key role in neurodegenerative disorders, including Parkinson’s disease (PD). Rice fermented with Monascus purpureus Went (Monascaceae) NTU 568 (red mould rice) was found to contain antioxidants, including dimerumic acid (DMA) and deferricoprogen (DFC).

Objective The effects of DMA and DFC on 6-hydroxydopamine (6-OHDA)-induced cytotoxicity and potential protective mechanisms in differentiated PC-12 pheochromocytoma cells were investigated.

Materials and methods DMA (0–60?μM) or DFC (0–10?μM) was co-treated with 6-OHDA (200?μM, 24?h exposure) in differentiated PC-12 cells. Cell viability and intercellular reactive oxygen species (ROS) were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and 2′,7′-dichlorofluorescein-diacetate (DCFH-DA) assays, respectively. Cell apoptosis was determined by DNA fragmentation analysis and propidium iodide staining by flow cytometry. Western blot analysis was used to measure the levels of cell protein expression.

Results DMA and DFC significantly increased cell viability to 72% and 81% in 6-OHDA-induced differentiated PC-12 cell cultures, respectively. Furthermore, DMA and DFC reduced 6-OHDA-induced formation of extracellular and intercellular ROS by 25% and 20%, respectively, and decreased NADPH oxidase-2 expression in differentiated PC-12 cells. DMA and DFC inhibited 6-OHDA-induced apoptosis and decreased activation of caspase-3 via regulation of Bcl-2-associated X protein (Bax) and Bcl-2 protein expression in differentiated PC-12 cells.

Conclusion DMA and DFC may protect against 6-OHDA toxicity by inhibiting ROS formation and apoptosis. These results showed that the metabolites from M. purpureus NTU 568 fermentation were potential therapeutic agents for PD induced by oxidative damage and should be encouraged for further research.