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	<title>Redox Health Blog</title>
	<atom:link href="http://www.redoxhealth.com/blog/?feed=rss2" rel="self" type="application/rss+xml" />
	<link>http://www.redoxhealth.com/blog</link>
	<description>The latest news in nutrition science - So you can live longer, faster, stronger</description>
	<pubDate>Wed, 22 Apr 2009 19:56:44 +0000</pubDate>
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		<title>Another great study on Beta Alanine</title>
		<link>http://www.redoxhealth.com/blog/?p=12</link>
		<comments>http://www.redoxhealth.com/blog/?p=12#comments</comments>
		<pubDate>Wed, 22 Apr 2009 19:56:44 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[Beta Alanine]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=12</guid>
		<description><![CDATA[Ollder people taking beta-alanine increased their physical working capacity in 90 days.
Muscle strength and stamina improved.]]></description>
			<content:encoded><![CDATA[<p>Here is another great study on Beta Alanine, again from the good people at the<strong> Journal of the International Society of Sports Nutrition.</strong> (J Int Soc Sports Nutr 2008;5:21)</p>
<p>They found that older people taking beta-alanine increased their physical working capacity in 90 days, with an increase in muscle strength and stamina.</p>
<p>The test group was 26 healthy men and women between 61 and 85 years old. They were randomly assigned to take beta-alanine, 800 mg three times per day, or placebo for 90 days. Physical work capacity, a measure of muscular endurance and aerobic power, was tested at the beginning and end of the trial.</p>
<p>67% of the people in the beta-alanine group experienced improvements in their physical working capacity between the beginning and end of the study. Muscle test measurements increased by an average of 28.6% in this group, but there was no change in the placebo group.</p>
<p>How is this relevant to athletes? This reinforces what studies have shown on athletes.  And we are getting older every day.</p>
<p>Thanks for reading.</p>
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		<title>That cell phones in front pockets can damage your sperm</title>
		<link>http://www.redoxhealth.com/blog/?p=39</link>
		<comments>http://www.redoxhealth.com/blog/?p=39#comments</comments>
		<pubDate>Tue, 24 Mar 2009 11:51:37 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[General Health]]></category>

		<category><![CDATA[oxidative stress]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=39</guid>
		<description><![CDATA[Now here is a study that most men (and their wives) of reproductive age should take to heart.
The Center for Reproductive Medicine at the Cleveland Clinic conducted a study that involved sampling the semen of 32 men, which exhibited similar sperm health.  The samples were kept at constant temperature and other similar conditions, while [...]]]></description>
			<content:encoded><![CDATA[<p>Now here is a study that most men (and their wives) of reproductive age should take to heart.</p>
<p>The Center for Reproductive Medicine at the Cleveland Clinic conducted a study that involved sampling the semen of 32 men, which exhibited similar sperm health.  The samples were kept at constant temperature and other similar conditions, while being split into a control group and a test group.  The test group was placed for an hour within 2.5 cm of a cell phone in talk mode, at 850 MHz, perhaps the most common cell phone frequency.</p>
<p>The exposure to the simulated cell transmission led to an increase in oxidative stress, with free radicals and oxidants being created at a higher rate and antioxidants being broken down.  Dr. Agarwal, The Center for Reproductive Medicine, said this stress equates to damaged sperm. Agarwal continued, &#8220;On average, there was an 85 percent increase in the amount of free radicals for all the subjects in the study. Free radicals have been linked to a variety of diseases in humans including cancer.&#8221;</p>
<p>Does this mean that we are all going to have mutant children and testicular cancer due to carrying a cell phone in our front pocket? Unlikely. But from a statisticians calculations, this will increase rates of both in a population.  There will be losers in the game of genetic chance.</p>
<p>An a broader scale I have to ask, what are to risks to by ears or brain by talking on a phone? We know that using a hands free device is recommended for this very reason.  And how are the myriad of various wireless transmissions all round us, which are growing in number, power, and frequency range every day? Time will tell.  And like global warming, it is likely too late to stop now.</p>
<p style="text-align: center;">
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		<title>L-Carnitine diminishes LDL oxidation</title>
		<link>http://www.redoxhealth.com/blog/?p=30</link>
		<comments>http://www.redoxhealth.com/blog/?p=30#comments</comments>
		<pubDate>Thu, 19 Mar 2009 13:24:56 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[Acetyl L-Carnitine]]></category>

		<category><![CDATA[oxidative stress]]></category>

		<category><![CDATA[Carnitine]]></category>

		<category><![CDATA[L-Carnitine]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=30</guid>
		<description><![CDATA[Why this is important: Oxidative stress can lead to higher risk for atherosclerosis. Oral administration of L-carnitine reduced oxidized LDL cholesterol levels in patients with type 2 diabetes.]]></description>
			<content:encoded><![CDATA[<p>The good people at the American Journal of Clinical Nutrition (Am J Clin Nutr. 2009;89(1):71-76) have published a L-Carnitine and Cholesterol study done by researchers at the University of Catania, Italy.</p>
<p>Why this is important: Oxidative stress can lead to higher risk for atherosclerosis.  A recent study at the University of Minnesota showed that people with high oxidation levels of  LDL cholesterol  are  more likely to develop metabolic syndrome – which can lead to a  increased risk of developing heart disease.</p>
<p>The U of M study involved more than 2,000 generally healthy people aged 33-45 (average age 40) for over for five years. Those with the highest levels of oxidized LDL had 3.5 times the risk of developing metabolic syndrome five years later.</p>
<p>When LDL cholesterol is oxidized it can lead to atherosclerosis, which is a plaque on the walls of arteries. Increased inflamation allows the plaque to build up much easier that in a void of inflammation. Causes of increased oxidative stress can range from smoking to running a marathon; a diet void of fruits and vegetables and high in processed or grilled foods.</p>
<p><strong>L-Carnitine</strong> continues to show up in diverse studies, reinforcing its many beneficial functions, from neurological protection and function, to fatty acid transport, cell membrane integrity, and now antioxidant effect on cholesterol.  I will be on the lookout for studies on LDL / L-Carnitine in healthy populations. (For more on L-Carnitine see our<a href="http://www.redoxhealth.com/carnitine.html" onclick=""> L-Carnitine</a> page.)</p>
<p>As they explain, &#8220;the production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular &#8216;reactive oxygen species&#8217; (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation.&#8221;</p>
<p>Excerpt from the Am J Clin Nutr: They evaluated the efficacy of L-carnitine on the reduction of oxidized low-density lipoprotein (LDL) cholesterol in patients with type 2 diabetes (Am J Clin Nutr. 2009;89(1):71-76). Eighty-one patients with diabetes were randomly assigned to one of two treatment groups for three months. The groups received either 2 g of L-carnitine once daily or a placebo. At the end of the study period, the L-carnitine-treated patients showed significant improvements compared to the placebo group. Oxidized LDL levels decreased by 15.1 compared with 3.0 U/L (P&lt;0.001). The results indicated that oral administration of L-carnitine reduced oxidized LDL cholesterol levels in patients with type 2 diabetes.</p>
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		<title>Plants may produce more Vitamin C now than in the past</title>
		<link>http://www.redoxhealth.com/blog/?p=46</link>
		<comments>http://www.redoxhealth.com/blog/?p=46#comments</comments>
		<pubDate>Tue, 17 Mar 2009 03:14:25 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[Vitamin C]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=46</guid>
		<description><![CDATA[Why does Vitamin C exist? How did it evolve? We often take for granted that all the things in and around us are the result of evolution, or going farther much farther back to get the actual elements, the result of a supernova.]]></description>
			<content:encoded><![CDATA[<p>Why does Vitamin C exist? How did it evolve?  We often take for granted that all the things in and around us are the result of evolution, or going farther much farther back to get the actual elements, the result of a supernova. I&#8217;ll save the chemistry of the universe for another post, however, because today I am focusing on vitamin C.</p>
<p>UCLA and Dartmouth scientists have identified a crucial enzyme in plant vitamin C synthesis. The discovery completes our understanding of the 10-step process by which plants convert glucose into vitamin C, which itself is crucial protective antioxidant in plants that produce it.</p>
<p>&#8220;If we can find ways to enhance the activity of this enzyme, it may be possible to engineer plants to make more vitamin C and produce better crops,&#8221; said ke,</p>
<p>When life on Earth began, explained Steven Clarke, there was almost no oxygen on Earth. &#8220;Two-billion years ago plants devised an efficient way to get sunlight to make sugar from carbon dioxide that produced oxygen as a waste product; that waste product probably killed off most of all living species at that time,&#8221; Clarke said. &#8220;The only organisms that survived developed defenses against it, and one of the best defenses is vitamin C. Plants learned how to make vitamin C to protect themselves.&#8221;</p>
<p>Clarke, who studies the biochemistry of aging, said the finding is an example of serendipity in science. &#8220;We hit on gold,&#8221; Clarke said, &#8220;because we now have a chance to improve human nutrition and to increase the resistance of plants to oxidative stress. Plants may grow better with more vitamin C, especially with more ozone in the atmosphere due to pollution.&#8221;</p>
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		<title>Beta Alanine supplementation may further enhance high intensity training, decrease body fat</title>
		<link>http://www.redoxhealth.com/blog/?p=9</link>
		<comments>http://www.redoxhealth.com/blog/?p=9#comments</comments>
		<pubDate>Sat, 14 Mar 2009 20:48:37 +0000</pubDate>
		<dc:creator>admin</dc:creator>
		
		<category><![CDATA[Antioxidants]]></category>

		<category><![CDATA[Beta Alanine]]></category>

		<category><![CDATA[Sports nutrition]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=9</guid>
		<description><![CDATA[The Study reinforces that Beta Alanine (and interval training) are winners. ]]></description>
			<content:encoded><![CDATA[<p>This is an interesting study on Beta Alanine. They wanted to test interval training and also the buffering effects of Beta Alanine on lactic acid or (H+) ions.  The Study reinforces that Beta Alanine (and interval training) are winners.</p>
<p>The below excerpt from the <em>Journal of the International Society of Sports Nutrition</em>: Intermittent bouts of high-intensity exercise result in diminished stores of energy substrates, followed by an accumulation of metabolites, promoting chronic physiological adaptations. In addition, beta-alanine has been accepted has an effective physiological hydrogen ion (H+) buffer.</p>
<p>Methods. Forty-six men (Age: 22.2 +/- 2.7 yrs; Ht: 178.1 +/- 7.4 cm; Wt: 78.7 +/- 11.9; VO2peak: 3.3 +/- 0.59 l * min-1) were assessed for peak O2 utilization (VO2peak), time to fatigue (VO2TTE), ventilatory threshold (VT), and total work done at 110% of pre-training VO2peak (TWD).</p>
<p>In a double-blind fashion, all subjects were randomly assigned into one either a placebo (PL - 16.5g dextrose powder per packet; n=18) or beta-alanine (BA - 1.5 g beta-alanine plus 15 g dextrose powder per packet; n=18) group. All subjects supplemented four times per day (total of 6g/day) for the first 21-days, followed by two times per day (3g/day) for the subsequent 21 days, and engaged in a total of six weeks of HIIT training consisting of 5-6 bouts of a 2:1 minute cycling work to rest ratio.</p>
<p>Results. Significant improvements in VO2peak, VO2TTE, and TWD after three weeks of training were displayed (p&lt;0.05).</p>
<p>Increases in VO2peak, VO2TTE, TWD and lean body mass were only significant for the BA group after the second three weeks of training. Conclusions.</p>
<p>The use of HIIT to induce significant aerobic improvements is effective and efficient. Chronic BA supplementation may further enhance HIIT, improving endurance performance and lean body mass.</p>
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		<title>Eat your Cheerios and Wheaties:  Whole Grain Intake reduces Inflammation</title>
		<link>http://www.redoxhealth.com/blog/?p=43</link>
		<comments>http://www.redoxhealth.com/blog/?p=43#comments</comments>
		<pubDate>Sat, 21 Feb 2009 15:16:18 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[Nutrition]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=43</guid>
		<description><![CDATA[Eat your Cheerios and Wheaties:  Whole Grain Intake reduces Inflammation]]></description>
			<content:encoded><![CDATA[<p>Eat your Cheerios and Wheaties, (unless you avoid gluten like I must).</p>
<p>OSLO, Norway—Whole grain intake was inversely linked to death from non-cardiovascular, non-cancer inflammatory diseases, according to a trial published in the June issue of the American Journal of Clinical Nutrition (85,6:1606-14, 2007).</p>
<p>Researchers from Institute of Basic Medical Sciences, University of Oslo, and School of Public Health, University of Minnesota, Minneapolis, monitored 27,312 postmenopausal women (between 55 to 69 years old), who took part in the Iowa Women’s Health Study. The women were followed for 17 years, during which 5,552 died. In analyzing the study data, researchers used a proportional hazards regression model, which was adjusted for age, smoking, adiposity, education, physical activity, and other dietary factors.</p>
<p>Compared with hazard ratios in women who rarely or never ate whole-grain foods, the hazard ratio was 0.69 for those who consumed four to seven servings weekly; 0.79 for 7.5 to 10.5 servings; 0.64 for 11 to 18.5 servings; and 0.66 for 19 servings. Previously reported inverse associations of whole-grain intake with total and coronary heart disease mortality persisted after 17 years of follow-up.</p>
<p>The researchers noted the reduction in inflammatory mortality associated with habitual whole-grain intake was larger than that previously reported for coronary heart disease and diabetes. They suggested oxidative stress reduction by constituents of whole grain is a likely mechanism for the protective effect because a variety of phytochemicals found in whole grains may directly or indirectly inhibit oxidative stress, and because oxidative stress is an inevitable consequence of inflammation.</p>
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		<title>Acute exercise increases expression of extracellular superoxide dismutase</title>
		<link>http://www.redoxhealth.com/blog/?p=26</link>
		<comments>http://www.redoxhealth.com/blog/?p=26#comments</comments>
		<pubDate>Wed, 14 Jan 2009 18:48:06 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[Sports nutrition]]></category>

		<category><![CDATA[oxidative stress]]></category>

		<category><![CDATA[Superoxide]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=26</guid>
		<description><![CDATA[More good stuff from the Source: Redox Report
Superoxide is biologically quite toxic and is deployed by the immune system to kill invading microorganisms, which is good.  This is why a bit of exercise is good.  It stresses the immune system.  But, the hard core athletes among us can overdo a good thing. [...]]]></description>
			<content:encoded><![CDATA[<p>More good stuff from the Source: <strong>Redox Report</strong></p>
<p>Superoxide is biologically quite toxic and is deployed by the immune system to kill invading microorganisms, which is good.  This is why a bit of exercise is good.  It stresses the immune system.  But, the hard core athletes among us can overdo a good thing. Superoxide is a byproduct of mitochondrial respiration and it can be inimical cellular health in high concentrations, such as during intense and prolonged exercise.  On to the study.</p>
<p>The abstract: Acute exercise increases expression of extracellular superoxide dismutase in skeletal muscle and the aorta.</p>
<p>Exercise dramatically increases oxygen consumption and causes oxidative stress. Superoxide dismutase (SOD) is important in the first-line defence mechanisms against oxidative stress. To investigate the effect of acute exercise on the expression of SOD, we examined the expression of mRNA for three SOD isozymes, in mice run on a treadmill to exhaustion. Six hours after exercise, the expression of extracellular SOD (EC-SOD) mRNA increased significantly in skeletal muscle and persisted for 24 h, whereas no change was observed for cytoplasmic and mitochondrial SOD mRNA. Moreover, acute exercise also induced EC-SOD mRNA in the aorta. These results suggest that a single bout of exercise is enough to augment the expression EC-SOD mRNA in skeletal muscle and the aorta, and may partly explain the beneficial effect of exercise.</p>
<p><strong>Redox Report</strong>(Volume 13, Number 5, October 2008 , pp. 213-216(4))</p>
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		<title>Oxidative stress increased in calcified, stenotic aortic valves</title>
		<link>http://www.redoxhealth.com/blog/?p=34</link>
		<comments>http://www.redoxhealth.com/blog/?p=34#comments</comments>
		<pubDate>Fri, 05 Dec 2008 13:57:02 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[oxidative stress]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=34</guid>
		<description><![CDATA[Excerpt of study published in J Am Coll Cardiol 2008;52:843-850: Oxidative stress is increased in atherosclerotic lesions and might play an important role in plaque progression and calcification.
Methods: Superoxide (dihydroethidium fluorescence and lucigenin-enhanced chemiluminescence), hydrogen peroxide (H2O2) (dichlorofluorescein fluorescence), and expression and activity of pro- and antioxidant enzymes were measured in normal valves from hearts [...]]]></description>
			<content:encoded><![CDATA[<p>Excerpt of study published in <strong>J Am Coll Cardiol 2008;52:843-850</strong>: Oxidative stress is increased in atherosclerotic lesions and might play an important role in plaque progression and calcification.</p>
<p><span style="text-decoration: underline;">Methods</span>: Superoxide (dihydroethidium fluorescence and lucigenin-enhanced chemiluminescence), hydrogen peroxide (H2O2) (dichlorofluorescein fluorescence), and expression and activity of pro- and antioxidant enzymes were measured in normal valves from hearts not suitable for transplantation and in stenotic aortic valves that were removed during surgical valve replacement.</p>
<p><span style="text-decoration: underline;">Conclusions</span>: This study provides evidence that oxidative stress is increased in calcified regions of stenotic human aortic valves. Increased oxidative stress is due at least in part to reduction in expression and activity of antioxidant enzymes and perhaps to uncoupled NOS activity. Based on this, mechanisms of oxidative stress differ between stenotic aortic valves and atherosclerotic arteries.</p>
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		<title>Increased oxidative stress during menstrual cycle</title>
		<link>http://www.redoxhealth.com/blog/?p=23</link>
		<comments>http://www.redoxhealth.com/blog/?p=23#comments</comments>
		<pubDate>Sun, 16 Nov 2008 14:01:08 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[oxidative stress]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=23</guid>
		<description><![CDATA[Here is another interesting study from the good people at Redox Report:
Changes of markers of oxidative stress during menstrual cycle
Authors: Karowicz-Bilinska, Agata1; Plodzidym, Magdalena2; Krol, Joanna2; Lewinska, Anna2; Bartosz, Grzegorz3
Source: Redox Report, Volume 13, Number 5, October 2008 , pp. 237-240(4)
Abstract:
The levels of urinary hydrogen peroxide and thiobarbituric acid reactive substances have been compared during [...]]]></description>
			<content:encoded><![CDATA[<p>Here is another interesting study from the good people at <strong>Redox Report</strong>:</p>
<p>Changes of markers of oxidative stress during menstrual cycle<br />
Authors: Karowicz-Bilinska, Agata1; Plodzidym, Magdalena2; Krol, Joanna2; Lewinska, Anna2; Bartosz, Grzegorz3<br />
Source: <strong>Redox Report</strong>, Volume 13, Number 5, October 2008 , pp. 237-240(4)</p>
<p>Abstract:<br />
The levels of urinary hydrogen peroxide and thiobarbituric acid reactive substances have been compared during the menstrual cycle of 12 regularly menstruating women. Higher level of both indices of oxidative stress (normalized with respect to creatinine content) were found in the luteal phase of the cycle. These results give further evidence for the usefulness of urinary hydrogen peroxide and thiobarbituric acid reactive substances as potential biomarkers of oxidative stress and for the antioxidant action of estrogens.</p>
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		<title>Antioxidant action in non-steroidal anti-inflammatory drugs</title>
		<link>http://www.redoxhealth.com/blog/?p=18</link>
		<comments>http://www.redoxhealth.com/blog/?p=18#comments</comments>
		<pubDate>Fri, 24 Oct 2008 11:48:36 +0000</pubDate>
		<dc:creator>T.Zuhlsdorf</dc:creator>
		
		<category><![CDATA[Antioxidants]]></category>

		<category><![CDATA[NSAID]]></category>

		<guid isPermaLink="false">http://www.redoxhealth.com/blog/?p=18</guid>
		<description><![CDATA[NSIADs possibly have an antioxidant action.]]></description>
			<content:encoded><![CDATA[<p>I&#8217;ve been buying Advil in the jumbo jugs ever since I started training for triathlons.  But little did I know that NSIADs possibly have an antioxidant action.  The notion came to me during a class I am taking at CU Boulder, about the Neurology of Aging. The professor said that there is some evidence that the anti-inflammation action from Ibuprofen and other NSIADs may diminish risk for Alzheimer&#8217;s disease.  I hit google right when I got home from class. So, on to the study, which is a little dense:</p>
<p>Singlet oxygen scavenging activity of non-steroidal anti-inflammatory drugs<br />
Authors: Costa, David1; Gomes, Ana1; Lima, José L.F.C.1; Fernandes, Eduarda1<br />
Source: <b>Redox Report</b>, Volume 13, Number 4, August 2008 , pp. 153-160(8)</p>
<p>Abstract:<br />
It has long been known that singlet oxygen (1O2) is generated during inflammatory processes. Once formed in substantial amounts, 1O2 may have an important role in mediating the destruction of infectious agents during host defense. On the other hand, 1O2 is capable of damaging almost all biological molecules and is particularly genotoxic, which gives a special relevance to the scavenging of this ROS throughout anti-inflammatory treatments. Considering that the use of non-steroidal anti-inflammatory drugs (NSAIDs) constitutes a first approach in the treatment of persistent inflammatory processes (due to their ability to inhibit cyclooxygenase), a putative scavenging activity of NSAIDs for 1O2 would also represent a significant component of their therapeutic effect. The aim of the present study was to evaluate the scavenging activity for 1O2 by several chemical families of NSAIDs. The results suggested that the pyrazole derivatives (dipyrone and aminopyrine) are, by far, the most potent scavengers of 1O2 (much more potent compared to the other tested NSAIDs), displaying IC50-values in the low micromolar range. There was a lack of activity for most of the arylpropionic acid derivatives tested, with only naproxen and indoprofen displaying residual activities, as for the oxazole derivative, oxaprozin. On the other hand, the pyrrole derivatives (tolmetin and ketorolac), the indolacetic acid derivatives (indomethacin, and etodolac), as well as sulindac and its metabolites (sulindac sulfide and sulindac sulfone) displayed scavenging activity in the high micromolar range. </p>
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