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pSimonkey
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20/12/2019 4:29 am  

Human & Experimental Toxicology, Vol. 26, No. 6, 509-518 (2007)
DOI: 10.1177/0960327107072392
© 2007 SAGE Publications
Nephrotoxicity and its prevention by taurine in tamoxifen induced oxidative stress in mice
Heena Tabassum

Immunotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi, India, Department of Biochemistry, U.C.M.S. & G.T.B. Hospital, Delhi, India

Suhel Parvez

Department of Neurology, University of Magdeburg, Magdeburg, Germany, [email protected]

Hasibur Rehman

Immunotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi, India

Basu Dev Banerjee

Department of Biochemistry, U.C.M.S. & G.T.B. Hospital, Delhi, India

Detlef Siemen

Department of Neurology, University of Magdeburg, Magdeburg, Germany

Sheikh Raisuddin

Immunotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi, India

tamoxifen (TAM) is an anti-neoplastic drug used for the treatment of breast cancer. It decreases the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in cells leading to tissue injury. The present study was undertaken to investigate modulatory effects of taurine on the nephrotoxicity of TAM with special reference to protection against disruption of nonenzymatic and enzymatic antioxidants. Oxidative stress was measured by renal lipid peroxidation (LPO) level, protein carbonyl (PC) content, reduced glutathione (GSH), activities of phase I and II drug metabolizing and antioxidant enzymes. TAM treatment resulted in a significant (P < 0.001) increase in LPO in kidney tissues as compared to control, while taurine pretreatment showed a significant decrease (P < 0.01) in the LPO in kidneys when compared with the TAM-treated group. Taurine + TAM group animals showed restoration in the level of cytochrome P450 content, activities of glutathione metabolizing enzymes viz., glutathione-S-transferase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase. Pretreatment of animals with taurine markedly attenuated, PC content, restored the depleted nonenzymatic and enzymatic antioxidants. These results clearly demonstrate the role of oxidative stress, and suggest a protective effect of taurine on TAM-induced nephrotoxicity in mice.


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jboldman
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20/12/2019 4:52 am  

very interesting. there are many long term studies of tamoxifen not showing adverse effects but this seems to indicate some. in any case this might be worth some investigation since taurine is easily obtained and used.

jb


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liftsiron
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20/12/2019 5:15 am  

Good find, some studies also indicate that taurine aids the heart muscle to stay healthy.

liftsiron is a fictional character and should be taken as such.


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jboldman
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20/12/2019 5:35 am  

hey lifts, post that up brother!

jb


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pSimonkey
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20/12/2019 5:54 am  

I found this

http://www.sciencedirect.com/scienc...9213bca8778ac67

Taurine protects the heart from neutrophil-induced reperfusion injury

Petra Raschke, Parwis Massoudy and Bernhard F. BeckerCorresponding Author Contact Information
Physiologisches Institut der Universität München, München, Germany
Received 7 September 1994; revised 1 March 1995; accepted 6 March 1995. ; Available online 14 January 2000.

Abstract

Deficiency of the amino acid taurine is implicated in various pathologic states of the heart. Besides other effects, taurine has been proposed to be an antioxidant. However, its benefit under conditions associated with the generation of reactive oxygen species in the heart has not been clearly demonstrated. To assess the potential of taurine to influence neutrophil-dependent reperfusion injury, a model was developed based on the isolated working guinea pig heart. After an initial work phase, hearts were subjected to 15 min of global ischemia. Reperfusion, in a nonworking mode, was carried out in the absence or presence of homologous neutrophils (PMN) and/or taurine. After 15 min, work was resumed and percentage recovery of function was determined another 20 min later. During the reperfusion phase, coronary venous effluent was collected to quantify release of lactate and glutathione, markers of ischemic challenge and redox-stress, respectively. Furthermore, direct effects of taurine on radical formation were investigated in a chemiluminescence assay. Control hearts without application of PMN or taurine had a postischemic recovery of external heart work (EHW) of 76%, in the presence of taurine (15 mM) recovery was 72%. The application of PMN for merely the first minute of reperfusion led to a significant decrease in recovery to 30%, PMN having no effect without a foregoing ischemia. When taurine was additionally applied during reperfusion, EHW recovered to 60%. Release of lactate and of oxidized glutathione (GSSG) did not differ between the groups. In contrast, effluent concentrations of reduced glutathione (GSH) were considerably elevated by the presence of PMN in the sample and remained high even after PMN-washout. Taurine tended to attenuate this PMN effect. At the 5th and 10th min of reperfusion, GSH release of individual hearts correlated inversely with postischemic recovery of EHW. Surprisingly, taurine, by itself, did not significantly alter glutathione release. However, taurine (15 mM) markedly reduced luminol-dependent chemiluminescence elicited by activated guinea pig PMN as well as by chemically generated hypochlorous acid and hydroxyl radicals, but not superoxide radicals. Our results demonstrate that taurine protects the heart from PMN-induced reperfusion injury and oxidative stress. Because respiratory burst activity of PMN was also significantly reduced in the presence of taurine, the beneficial effect appears to be mediated by antioxidative properties of taurine.


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jboldman
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20/12/2019 6:14 am  

nice find, will add that to my heart archives.

jb


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pSimonkey
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20/12/2019 6:39 am  

and also...

Taurine Supplementation Reduces Oxidative Stress and Improves Cardiovascular Function in an Iron-Overload Murine Model
Gavin Y. Oudit, MSc, MD; Maria G. Trivieri, MD; Neelam Khaper, PhD; Taneya Husain, BSc; Greg J. Wilson, MD; Peter Liu, MD; Michael J. Sole, MD; Peter H. Backx, DVM, PhD

From the Departments of Physiology and Medicine, Toronto General Hospital, University Health Network, Heart and Stroke/Richard Lewar Centre of Excellence (G.Y.O., M.G.T., N.K., P.L., M.J.S., P.H.B.), and the Department of Pathology, Hospital for Sick Children (T.H., G.J.W.), University of Toronto, Toronto, Ontario, Canada.

Correspondence to Dr Michael Sole, MD, FRCP(C), FACC, FAHA, Professor of Medicine and Physiology, University of Toronto, Division of Cardiology, University Health Network and Mount Sinai Hospital, Room 13-212 EN, 200 Elizabeth St, Toronto, Ontario, Canada, M5G 2C4. E-mail [email protected]

Received October 23, 2002; de novo received October 16, 2003; revision received December 15, 2003; accepted January 7, 2004.

Background— Iron overload has an increasing worldwide prevalence and is associated with significant cardiovascular morbidity and mortality. Elevated iron levels in the myocardium lead to impaired systolic and diastolic function and elevated oxidative stress. Taurine accounts for 25% to 50% of the amino acid pool in myocardium, possesses antioxidant properties, and can inhibit L-type Ca2+ channels. Thus, we hypothesized that this agent would reduce the cardiovascular effects of iron overload.

Methods and Results— Iron-overloaded mice were generated by intraperitoneal injection of iron either chronically (5 days per week for 13 weeks) or subacutely (5 days per week for 4 weeks). Iron overload causes increased mortality, elevated oxidative stress, systolic and diastolic dysfunction, hypotension, and bradycardia. Taurine supplementation increased myocardial taurine levels by 45% and led to reductions in mortality and improved cardiac function, heart rate, and blood pressure in iron-overloaded mice. Histological examination of the myocardium revealed reduced apoptosis and interstitial fibrosis in iron-overloaded mice supplemented with taurine. Taurine mediated reduced oxidative stress in iron-overloaded mice along with attenuation of myocardial lipid peroxidation and protection of reduced glutathione level.

Conclusions— These results demonstrate that treatment with taurine reduces iron-mediated myocardial oxidative stress, preserves cardiovascular function, and improves survival in iron-overloaded mice. The role of taurine in protecting reduced glutathione levels provides an important mechanism by which oxidative stress–induced myocardial damage can be curtailed. Taurine, as a dietary supplement, represents a potential new therapeutic agent to reduce the cardiovascular burden from iron-overload conditions.


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jboldman
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20/12/2019 6:58 am  

keep them coming!

jb


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liftsiron
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20/12/2019 7:26 am  

I seen the second one, I will look for others, I have seen at least a half-dozen or so.

liftsiron is a fictional character and should be taken as such.


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