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#1 gamesguru

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Posted 29 September 2016 - 11:08 PM

Sorry for the long quote block and lack of explanation.

Effects of catechin and   epicatechin   on superoxide dismutase and glutathione peroxidase activity, in vivo.
Simos YV1, Verginadis II, Toliopoulos IK, Velalopoulou AP, Karagounis IV, Karkabounas SC, Evangelou AM. (2012)

OBJECTIVES: The objective of this study was to investigate the effects of catechin and epicatechin on the activity of the endogenous antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) (as well as the total antioxidant capacity (TAC)) of rats after intra-peritoneal (i.p.) administration.
METHODS: Twenty-four Wistar rats were randomly divided into two groups: the experimental group which was administered daily with a 1:1 mixture of epicatechin and catechin at a concentration of 23 mg/kg body weight for 10 days and the control group which was injected daily with an equal amount of saline. Blood and urine samples were collected before and after the administration period, as well as 10 days after (follow-up).
RESULTS: Intra-peritoneal administration of catechins led to a potent decrease in GPx levels and a significant increase in SOD levels. TAC was significantly increased in plasma and urine. Malonaldehyde levels in urine remained stable. In the animals treated with catechins, SOD activity showed a moderate negative correlation with GPx activity.
DISCUSSION: Boosting the activity of the antioxidant enzymes could be a potential adjuvant approach for the treatment of the oxidative stress-related diseases.

Protective Role of   Turmeric   in Manganese-Induced Oxidative Alterations in Rat Brain
Darshika Nigam, Vibha Rani, Kalpana Singh (2013)

Turmeric powder obtained from the rhizomes of Curcuma longa Linn., has been traditionally recognized for treatment of several diseases. Overexposure to manganese (Mn) results in a neurological disorder, termed manganism which shares a similar phenotype to Parkinson's disease. The present study explores the protective effect of turmeric against the toxicity of manganese (Mn) in adult albino male rat brain. Rats were divided into four groups. Group I rats served as control. Group II rats received turmeric (1g/kg body weight/day, orally) for 45 days. Group III rats were received Mn as MnCl2 (8mg/Kg body weight/day), intraperitoneally for 15 days. Group IV rats were orally received turmeric for 45 days. Besides turmeric, group IV rats were also received Mn as MnCl2 (8mg/Kg body weight/day, intraperitoneally) for last 15 days. Levels of reactive oxygen species, lipid peroxidation potential, conjugated dienes, blood-brain barrier permeability, glutathione reductase and glutathione peroxidase were significantly increased, however lower levels of superoxide dismutase, reduced glutathione and membrane fluidity were observed in brain of group III. There was no change found in the activity of catalase in brain of any of the experimental groups. These changes were ameliorated in group IV. The study suggests that turmeric exhibits neuroprotection against free radical-mediated neurotoxicity of Mn.

The effects of   ellagic acid   and  vitamin E  succinate on antioxidant e nzymes activities and glutathione levels in different brain regions of rats after subchronic exposure to TCDD.
Hassoun EA1, Vodhanel J, Holden B, Abushaban A. (2006)

Ellagic acid (EA) and vitamin E succinate (VES) were previously shown to protect against 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD)-induced reactive oxygen species (ROS) overproduction in certain brain regions of rats after subchronic exposure. The current study was designed to assess the modulation of antioxidant enzyme activities and glutathione (GSH) levels as protective measures for VES and EA against TCDD-induced ROS overproduction in four regions of rat brain. TCDD was administered to groups of rats at a daily dose of 46 ng/kg for 90 d. EA and VES were administered to some other groups of rats either alone or simultaneously with TCDD, every other day for 90 d. At the end of the treatment period, animals were sacrificed and brain regions were dissected, including cerebral cortex (Cc), hippocampus (H), cerebellum ©, and brainstem (Bs), for assay of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as GSH levels. While treatment of rats with VES alone or in combination with TCDD resulted in significant increases in SOD and CAT activities in different brain regions, treatment with EA resulted in a significant rise in total GSH levels and GSH-Px activity in those regions. Results may suggest antioxidant modulation by VES and EA as a mechanism for the previously observed protection by these compounds against TCDD-induced ROS overproduction in brain. Data also indicate there are two different pathways in the protection provided by the two antioxidants.

Effects of  lycopene  and proanthocyanidins on hepatotoxicity in duced by mercuric chloride in rats.
Deng Y1, Xu Z, Liu W, Yang H, Xu B, Wei Y. (2012)

To evaluate the protective potential of lycopene (Lyc) and proanthocyanidins (PCs) against mercuric chloride (HgCl(2))-induced hepatotoxicity, the study focused on the mechanism of oxidative stress. Firstly, the rats were subcutaneously (s.c.) injected with 0, 2.2, 4.4, and 8.8 μmol/kg HgCl(2). Additionally, 40 mg/kg Lyc and 450 mg/kg PCs were given to the rats intragastrically (i.g.) before exposure to 8.8 μmol/kg HgCl(2). Then, body weight, liver weight coefficient, mercury (Hg) contents, histological feature, ultrastructure, apoptosis, reactive oxygen species (ROS), glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and malondialdehyde (MDA) in the liver were measured. Lactate dehydrogenase (LDH) and alanine transaminase (ALT) in serum were determined. After exposure to different concentrations of HgCl(2), it was found that Hg contents, pathological and ultrastructure injury, activities of LDH and ALT, apoptosis, and levels of ROS, GSH, and MDA increased and the activities of SOD and GSH-Px decreased in a concentration-dependent manner. Further investigation found that pretreatment with Lyc and PCs inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity. We concluded that Lyc and PCs had hepatoprotective effects on HgCl(2)-induced toxicity by antagonizing oxidative stress in rat liver.

  Flavonoids   increase the intracellular glutathione level by transactivation of the gamma-glutamylcysteine synthetase catalytical subunit promoter.
Myhrstad MC1, Carlsen H, Nordström O, Blomhoff R, Moskaug JØ. (2002)

Fruits and vegetables protect against cancer by so far not well-characterized mechanisms. One likely explanation for this effect is that dietary plants contain substances able to control basic cellular processes such as the endogenous defense against oxidative stress. Oxidative stress is pivotal in many pathological processes and reduced oxidative stress is implicated in prevention of disease. Our results demonstrate that extract from onion and various flavonoids induce the cellular antioxidant system. Onion extract and quercetin were able to increase the intracellular concentration of glutathione by approximately 50%. Using a reporter construct where reporter expression is driven by the gamma-glutamylcysteine synthetase (GCS) heavy subunit (GCS(h)) promoter we show that onion extract, quercetin, kaempferol, and apigenin increased reporter gene activity, while a fourth flavonoid, myricetin and sugar conjugates of quercetin were unable to increase reporter expression. Quercetin was also able to induce a distal part of the GCS(h) promoter containing only two antioxidant-response/electrophile-response elements (ARE/EpRE). Our data strongly suggest that flavonoids are important in the regulation of the intracellular glutathione levels. This effect may be exerted in part through GCS gene regulation, and may also contribute to the disease-preventing effect of fruits and vegetables.

  Sulforaphane   as an inducer of glutathione prevents oxidative stress-induced cell death in a dopaminergic-like neuroblastoma cell line.
Tarozzi A1, Morroni F, Merlicco A, Hrelia S, Angeloni C, Cantelli-Forti G, Hrelia P. (2009)

The total GSH depletion observed in the substantia nigra (SN) appears to be responsible for subsequent oxidative stress (OS), mitochondrial dysfunction, and dopaminergic cell loss in patients with Parkinson's disease. A strategy to prevent the OS of dopaminergic cells in the SN may be the use of chemopreventive agents as inducers of endogenous GSH, antioxidant and phase 2 enzymes. In this study, we demonstrated that treatment of the dopaminergic-like neuroblastoma SH-SY5Y cell line with sulforaphane (SF), a cruciferous vegetables inducer, resulted in significant increases of total GSH level, NAD(P)H : quinone oxidoreductase-1, GSH-transferase and -reductase, but not GSH-peroxidase, catalase and superoxide dismutase activities. Further, the elevation of GSH levels, GSH-transferase and NAD(P)H:quinone oxidoreductase-1 activities was correlated to an increase of the resistance of SH-SY5Y cells to toxicity induced by H(2)O(2) or 6-hydroxydopamine (6-OHDA). The pre-treatment of SH-SY5Y cells with SF was also shown to prevent various apoptotic events (mitochondrial depolarization, caspase 9 and 3 activation and DNA fragmentation) and necrosis elicited by 6-OHDA. Further, the impairment of antioxidant capacity and reactive oxygen species formation at intracellular level after exposure to 6-OHDA was effectively counteracted by pre-treatment with SF. Last, both the cytoprotective and antioxidant effects of SF were abolished by the addition of buthionine sulfoximine supporting the main role of GSH in the neuroprotective effects displayed by SF. These findings show that SF may play a role in preventing Parkinson's disease.


Sulforaphane is anticonvulsant and improves mitochondrial function.
Carrasco-Pozo C1,2, Tan KN1, Borges K1. (2015)

The nuclear factor erythroid 2-related factor 2 pathway (Nrf2) has been previously identified to protect the brain against various impacts. Here, we investigated the effect of the Nrf2 activator sulforaphane in various seizure models and hippocampal mitochondrial bioenergetics. We found that daily injections of sulforaphane for 5 days elevated the seizure thresholds to 6 Hz stimulation and fluorothyl-, but not pentylenetetrazole-induced tonic seizures and protected mice against pilocarpine-induced status epilepticus (SE). Also, sulforaphane increased the antioxidant defences within hippocampal formations and blood plasma. In addition, sulforaphane treatment reduced the extent of hippocampal lipid peroxidation 24 h post-SE and protected hippocampal mitochondria against SE-induced reduction in state 2 and uncoupler-stimulated state 3 respiration. SE-mediated partial loss of rotenone-sensitive and complex II-driven respiration was reduced, consistent with the enhanced activities of complexes I and II in sulforaphane-treated SE mice. In mitochondria isolated from both no SE and SE mice, sulforaphane increased state 3 respiration and respiration linked to ATP synthesis, which may contribute to its anticonvulsant and antioxidant effects by providing more ATP for cellular vital and protective functions. However, sulforaphane did not prevent SE-induced hippocampal cell death. In conclusion, sulforaphane and/or Nrf2 activation are viable anticonvulsant strategies, which are antioxidant and enhance mitochondrial function, especially the ability to produce ATP. Sulforaphane was anticonvulsant in two acute mouse models of epilepsy and protected mice against pilocarpine-induced status epilepticus (SE). We also found antioxidant effects of sulforaphane in mouse plasma and hippocampal formations, exhibited by increased catalase and superoxide dismutase (SOD) activity, as well as increased abilities of hippocampal mitochondria to produce ATP. These effects likely underlie sulforaphane's anticonvulsant mechanisms of action.

Mechanism of Action of Sulforaphane as a Superoxide Radical Anion and Hydrogen Peroxide Scavenger by Double Hydrogen Transfer: A Model for Iron Superoxide Dismutase
Ajit Kumar Prasad and P.C. Mishra (2015)

The mechanism of action of sulforaphane as a scavenger of superoxide radical anion (O2•–) and hydrogen peroxide (H2O2) was investigated using density functional theory (DFT) in both gas phase and aqueous media. Iron superoxide dismutase (Fe-SOD) involved in scavenging superoxide radical anion from biological media was modeled by a complex consisting of the ferric ion (Fe3+) attached to three histidine rings. Reactions related to scavenging of superoxide radical anion by sulforaphane were studied using DFT in the presence and absence of Fe-SOD represented by this model in both gas phase and aqueous media. The scavenging action of sulforaphane toward both superoxide radical anion and hydrogen peroxide was found to involve the unusual mechanism of double hydrogen transfer. It was found that sulforaphane alone, without Fe-SOD, cannot scavenge superoxide radical anion in gas phase or aqueous media efficiently as the corresponding reaction barriers are very high. However, in the presence of Fe-SOD represented by the above-mentioned model, the scavenging reactions become barrierless, and so sulforaphane scavenges superoxide radical anion by converting it to hydrogen peroxide efficiently. Further, sulforaphane was found to scavenge hydrogen peroxide also very efficiently by converting it into water. Thus, the mechanism of action of sulforaphane as an excellent antioxidant has been unravelled.

Effects of   garlic and onion   oils on glutathione peroxidase activity, the ratio of reduced/oxidized glutathione and ornithine decarboxylase induction in isolated mouse epidermal cells treated with tumor promoters.
Perchellet JP, Perchellet EM, Abney NL, Zirnstein JA, Belman S. (1986)

Garlic oil, onion oil and one of its constituents, dipropenyl sulfide, all increase, to diverse degrees, glutathione (GSH) peroxidase (GSH:H2O2 oxidoreductase, EC activity in isolated epidermal cells incubated in the presence or absence of the potent tumor promoter 12-0-tetradecanoylphorbol-13-acetate (TPA). The stimulatory effects of these oils on epidermal GSH peroxidase activity are concentration-dependent and long-lasting, and thus, abolish totally the prolonged inhibitory effect of TPA on this enzyme. Moreover, garlic oil (5 micrograms/ml) inhibits by about 50% TPA-induced ornithine decarboxylase (ODC, L-ornithine carboxy-lyase, EC activity in the same epidermal cell system. This concentration of garlic oil also increases remarkably GSH peroxidase activity and inhibits ODC induction in the presence of various nonphorbol ester tumor promoters. Since the same oil treatments inhibit dramatically the sharp decline in the intracellular ratio of reduced (GSH)/oxidized (GSSG) glutathione caused by TPA, it is suggested that some of the inhibitory effects of garlic and onion oils on skin tumor promotion may result from their enhancement of the natural GSH-dependent antioxidant protective system of the epidermal cells.

Diallyl disulfide ameliorates gentamicin-induced oxidative stress and nephropathy in rats.
Pedraza-Chaverrí J1, González-Orozco AE, Maldonado PD, Barrera D, Medina-Campos ON, Hernández-Pando R. (2003)

Experimental evidences suggest a role of reactive oxygen species in gentamicin-induced nephropathy in rats. Therefore, we investigated if diallyl disulfide, a garlic-derived compound with antioxidant properties, has a renoprotective effect in this experimental model. Four groups of rats were studied: (1) control, (2) gentamicin treated subcutaneously with gentamicin (70 mg/kg/12 h/4 days), (3) diallyl disulfide treated intragastrically with diallyl disulfide (50 mg/kg/24 h/4 days), and (4) gentamicin + diallyl disulfide treated with gentamicin + diallyl disulfide. Gentamicin induced (a) nephrotoxicity, (b) increase in renal oxidative stress, and © decrease in the activity of manganese superoxide dismutase, glutathione peroxidase, and glutathione reductase. Diallyl disulfide ameliorated these changes induced by gentamicin. The mechanism by which diallyl disulfide has a renoprotective effect in gentamicin-induced acute renal failure in rats may be related, at least in part, to the amelioration in the oxidative stress and the preservation in the activity of the antioxidant enzymes in kidney.

Neuropharmacological Review of the Nootropic Herb   Bacopa   monnieri
Sebastian Aguiarcorresponding author and Thomas Borowski (2013)

Anbarasi et al.56 assessed the neuroprotective role of bacoside A against OS in the brains of rats exposed to cigarette smoke by measuring concentrations of enzymatic and non-enzymatic anti-oxidants as well as trace elements. The researchers administered 10 mg/kg aqueous bacoside A gavage daily and found that BM significantly increased brain levels of glutathione, vitamin C, vitamin E, and vitamin A in rats exposed to cigarette smoke (perhaps an anti-oxidant conservation effect). Bacoside A administration increased the activities of superoxide dismutase (SOD), catalase, GPx, and GSR. As a result, the levels of glutathione (primary endogenous anti-oxidant conjugate) in the brain were significantly increased as well. The researchers found that cigarette smoke depletes zinc and selenium levels in the brain, which is especially problematic because zinc is a SOD co-factor and selenium is a GPx co-factor. Administration of bacoside A also restored zinc and selenium levels.

Alleviating exercise-induced muscular stress using neat and processed   bee pollen  : oxidative markers, mitochondrial enzymes, and myostatin expression in rats
Sameer Ketkara, Atul Rathorea, Amit Kandharea, Sathiyanarayanan Lohidasana (2015)

Background: The current study was designed to investigate the influence of monofloral Indian mustard bee pollen (MIMBP) and processed monofloral Indian mustard bee pollen (PMIMBP) supplementation on chronic swimming exercise-induced oxidative stress implications in the gastrocnemius muscle of Wistar rats.
Methods: MIMBP was processed with an edible lipid-surfactant mixture (Captex 355:Tween 80) to increase the extraction of polyphenols and flavonoid aglycones as analyzed by UV spectroscopy and high performance liquid chromatography-photo diode array. Wistar rats in different groups were fed with MIMBP or PMIMBP supplements at a dose of 100 mg/kg, 200 mg/kg and 300 mg/kg individually, while being subjected to chronic swimming exercise for 4 weeks (5 d/wk). Various biochemical [superoxide dismutase (SOD), glutathione (GSH), malonaldehyde (MDA), nitric oxide (NO), and total protein content], mitochondrial (Complex I, II, III, and IV enzyme activity), and molecular (myostatin mRNA expression) parameters were monitored in the gastrocnemius muscle of each group.
Results: Administration of both MIMBP (300 mg/kg) and PMIMBP (100 mg/kg, 200 mg/kg, and 300 mg/kg) wielded an antioxidant effect by significantly improving SOD, GSH, MDA, NO, and total protein levels. Further MIMBP (300 mg/kg) and PMIMBP (200 mg/kg and 300 mg/kg) significantly improved impaired mitochondrial Complex I, II, III, and IV enzyme activity. Significant down-regulation of myostatin mRNA expression by MIMBP (300 mg/kg) and PMIMBP (200 mg/kg and 300 mg/kg) indicates a muscle protectant role in oxidative stress conditions.
Conclusion: The study establishes the antioxidant, mitochondrial upregulatory, and myostatin inhibitory effects of both MIMBP and PMIMBP in exercise-induced oxidative stress conditions, suggesting their usefulness in effective management of exercise-induced muscular stress. Further, processing of MIMBP with an edible lipid-surfactant mixture was found to improve the therapeutic efficiency of pollen.

Effects of administration of the standardized Panax   ginseng   extract G115 on hepatic antioxidant function after exhaustive exercise.
Voces J1, Alvarez AI, Vila L, Ferrando A, Cabral de Oliveira C, Prieto JG. (1999)

The effect of prolonged treatment with the standardized Panax ginseng extract G115 on the antioxidant capacity of the liver was investigated. For this purpose, rats that had received G115 orally at different doses for 3 months and untreated control rats were subjected to exhaustive exercise on a treadmill. A bell-shaped dose response on running time was obtained. The results showed that the administration of G115 significantly increases the hepatic glutathione peroxidase activity (GPX) and the reduced glutathione (GSH) levels in the liver, with a dose-dependent reduction of the thiobarbituric acid reactant substances (TBARS). After the exercise, there is reduced hepatic lipid peroxidation, as evidenced by the TBARS levels in both the controls and the treated animals. The GPX (glutathione peroxidase) and SOD (superoxide dismutase) activity are also significantly increased in the groups receiving G115, compared with the controls. The hepatic transaminase levels, ALT (Alanine-amino-transferase) and AST (Aspartate-amino-transferase), in the recuperation phase 48 h after the exercise, indicate a clear hepatoprotective effect related to the administration of the standardized Panax ginseng extract G115. At hepatic level, G115 increases the antioxidant capacity, with a marked reduction of the effects of the oxidative stress induced by the exhaustive exercise.

  Royal Jelly   Constituents Increase the Expression of Extracellular Superoxide Dismutase through Histone Acetylation in Monocytic THP-1 Cells.
Makino J1, Ogasawara R1, Kamiya T1, Hara H1, Mitsugi Y1, Yamaguchi E1, Itoh A1, Adachi T1. (2016)

Extracellular superoxide dismutase (EC-SOD) is one of the main SOD isozymes and plays an important role in the prevention of cardiovascular diseases by accelerating the dismutation reaction of superoxide. Royal jelly includes 10-hydroxy-2-decenoic acid (10H2DA, 2), which regulates the expression of various types of genes in epigenetics through the effects of histone deacetylase (HDAC) antagonism. The expression of EC-SOD was previously reported to be regulated epigenetically through histone acetylation in THP-1 cells. Therefore, we herein evaluated the effects of the royal jelly constituents 10-hydroxydecanoic acid (10HDA, 1), sebacic acid (SA, 3), and 4-hydroperoxy-2-decenoic acid ethyl ester (4-HPO-DAEE, 4), which is a derivative of 2, on the expression of EC-SOD in THP-1 cells. The treatment with 1 mM  or 3 or 100 μM  increased EC-SOD expression and histone H3 and H4 acetylation levels. Moreover, the enrichment of acetylated histone H4 was observed in the proximal promoter region of EC-SOD and was caused by the partial promotion of ERK phosphorylation (only 4) and inhibition of HDAC activities, but not by the expression of HDACs. Overall, 4 exerted stronger effects than 1, 2, or 3 and has potential as a candidate or lead compound against atherosclerosis.

Combined effects of   methionine   and  kiwi  fruit on paracetamol induced  liver injury
R.M. Nagib (2013)

In the present study, the effects of methionine and kiwi fruit powder on paracetamol induced liver damage were evaluated. Forty adult male of white albino rats (Wistar rats strain) were randomly classified into five groups (8 rats each). The first group kept as control negative. The rest rats were administered paracetamol to induce liver injury and classified into control positive and treated groups which were methionine, kiwi powder and kiwi powder with methionine groups. Liver aspartate and alanine aminotransferase (AST, ALT) activity, alkaline phosphatase (ALP) and gamma glutamyle transferase (GT) enzymes as well as total bilirubin, total protein, albumin and globulin were determined in serum. Liver lipids parameters (cholesterol, total lipids, triglyceride and glycogen), Liver antioxidant enzymes (superoxide dismutase, SOD, glutathione peroxidase, GPX, glutathione S-transferase, GST and catalase) were estimated. Paracetamol administration showed a significant decrease in nutritional results; liver antioxidant enzymes; liver triglyceride and liver glycogen but showed a significant increase in liver and renal function parameters enzymes and MDA as shown in control positive group. Liver injured rats groups which fed diet contains methionine or kiwi powder or methionine with kiwi powder had a significant increase in body weight gain, food intake and feed efficiency ratio (FER) compared to rats of control positive group. Consumption of methionine with kiwi powder showed a significant improves of liver function enzymes, liver antioxidant enzymes and liver lipid pattern compared to rats of control positive group that is may be due to its augmenting endogenous antioxidant mechanisms

Protective effects from  carnosine  and histidine on acetaminophen-induced liver i njury.
Yan SL1, Wu ST, Yin MC, Chen HT, Chen HC. (2009)

Protective effects of carnosine or histidine against acetaminophen-induced hepatotoxicity in Balb/cA mice were examined. Each compound, at 0.5, 1, or 2 g/L, was added into the drinking water for 4 wk. Acute liver injury was induced by acetaminophen treatment intraperitoneally (i.p. 350 mg/kg body weight). Acetaminophen treatment significantly depleted hepatic GSH and ascorbic acid levels, increased hepatic level of malonyldialdehyde (MDA), reactive oxygen species (ROS), and oxidized glutathione (GSSG), as well as decreased hepatic activity of glutathione peroxidase (GPX), catalase, and superoxide dismutase (SOD) (P < 0.05). However, the pre-intake of carnosine or histidine significantly alleviated acetaminophen-induced oxidative stress by increasing GSH content, decreasing MDA, ROS, and GSSG formations, and retaining activity of GPX, catalase, and SOD in liver (P < 0.05). The pre-intake of these compounds also significantly retarded subsequent acetaminophen-induced increase of cytochrome P450 2E1 activity (P < 0.05). Acetaminophen treatment increased the hepatic levels of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha, and monocyte chemoattractant protein (MCP)-1 (P < 0.05). The pre-intake of carnosine or histidine significantly diminished acetaminophen-induced elevation of these cytokines (P < 0.05). The impact of these compounds on mRNA expression of GPX, TNF-alpha, and MCP-1 indicated that these compounds could act at a transcription level. These results support that carnosine and histidine are potent hepatoprotective agents.

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#2 jack black

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Posted 30 September 2016 - 12:25 PM

Do you have a problem with SOD and oxidation? Do you take them all.

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#3 gamesguru

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Posted 30 September 2016 - 03:12 PM

No, I don't take everything on the list lol.  I take everything but the methionine, carnosine, and histidine.  But yes, I do have a problem with oxidation.  Don't we all?  It's not going to cure any of these diseases, just addressing endogenous antioxidant defenses, but you can hardly argue that it would hurt.

Reduced superoxide dismutase in lung cells of patients with asthma.
Smith LJ1, Shamsuddin M, Sporn PH, Denenberg M, Anderson J. (1997)

Lung cells recovered from symptomatic patients with asthma generate increased amounts of reactive oxygen species (ROS). Animal and in vitro studies indicate that ROS can reproduce many of the features of asthma. The ability of ROS to produce the clinical features of asthma may depend on an individual's lung antioxidant defenses. Patients with asthma are reported to have reduced antioxidant defenses in peripheral blood, but little is known about the antioxidant defenses of their lung cells. To define lung cell antioxidant defenses in asthma, the glutathione concentration and the glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase (SOD) activities were measured in cells recovered by bronchoalveolar lavage (BAL cells) and by bronchial brushing (bronchial epithelial cells, HBEC) from normal subjects and patients with asthma. Superoxide dismutase activity was reduced 25% in BAL cells (p < .05) and nearly 50% in HBEC (p < .02) from patients with asthma. Alterations in the other antioxidants were not identified. A direct relationship was found between airway reactivity to methacholine, measured as PC(20)FEV(1), and HBEC SOD activity (r2 = 89; p < .005), but not between airway reactivity and the other antioxidants. The finding of reduced SOD activity in lung cells of patients with asthma suggests that diminished SOD activity serves as a marker of the inflammation characterizing asthma. Alternatively, it may play a role in the development or severity of the disease.

Role of Reactive Oxygen Species and Antioxidants in Atopic Dermatitis
N. Sivaranjani, S. Venkata Rao, and G. Rajeev (2013)

Background: In humans, oxidative stress is involved in many diseases such as atherosclerosis, Parkinson’s disease, heart failure, myocardial infarction, Alzheimer’s disease, Fragile X syndrome and chronic fatigue syndrome. Atopic dermatitis (AD), also known as atopic eczema, is a non-contagious, relapsing inflammatory skin disease which is characterized by eczema and pruritus. The skin reacts abnormally to irritants, food and environmental allergens and it becomes very itchy, which leads to scratching, redness and flaky skin. Very little study has been done to find out the relationship between oxidative stress and Atopic dermatitis.
Aim: The aim of our work was to evaluate the status of oxidative stress in patients of Atopic dermatitis in comparison with healthy control subjects.
Material and Methods: Twenty five patients of known Atopic dermatitis and 25 normal healthy controls of same age group were included in the study. Estimations of oxidants like Malondialdehyde (MDA), enzymatic antioxidants like Superoxide dismutase (SOD), Catalase, Glutathione peroxidase (GPX) and non-enzymatic antioxidants like reduced Glutathione (GSH), Vitamin A, Vitamin E and Vitamin C were done to assess the oxidative stress.
Results: Atopic dermatitis patients were more prone to damage caused by Reactive Oxygen Species (ROS) or Oxidants, than controls, which was evident from an increase of Malondialdehyde and a decrease of enzymatic and non enzymatic Antioxidants.
Conclusion: Antioxidants may possibly be beneficial in the treatment of Atopic dermatitis, which must be substantiated by further studies.

Catalase, superoxide dismutase and glutathione peroxidase activity in neutrophils of sham-operated and olfactory-bulbectomised rats following chronic treatment with desipramine and lithium chloride.
Song C1, Killeen AA, Leonard BE. (1994)

In the olfactory-bulbectomised rat model of depression, neutrophil phagocytosis was significantly decreased and phagocytosis started later in comparison to sham-operated animals. Both desipramine and lithium chloride treatment significantly reversed the depressed neutrophil phagocytosis and shortened the time to commencement of phagocytosis in drug-treated bulbectomised rats. The catalase and glutathione peroxidase (GSH-PX) activities in bulbectomised rats were decreased, while superoxide dismutase (SOD) was significantly increased. Chronic desipramine and lithium chloride treatment slightly improved catalase activity in the bulbectomised rats. Desipramine significantly reversed the reduction in activity of GSH-PX, but failed to reverse the increased activity of SOD. In contrast, lithium chloride significantly reversed SOD activity to normal values, without affecting GSH-PX activity in the bulbectomised rats.

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