Antioxidative effect of melatonin on DNA and erythrocytes against free-radical-induced oxidation

Zhao, Feng; Liu, Zai‐Qun; Wu, Di

doi:10.1016/j.chemphyslip.2007.10.002

Cited by 39 publications

(37 citation statements)

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“…Meanwhile, melatonin showed a significant degree of protection of DNA in the range of chronic exposure, from 16.6 to 33.2 days, mainly due to its ability of scavenging the radical species, as noted in subsequent studies, which showed that melatonin is a dose-dependent protective agent against DNA oxidative damage ( Zhao et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Melatonin Protective Role in Mouse Cauda Epipidymal Spermatozoa Damage Induced by Sodium Arsenite

et al. 2013

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SUMMARY:We evaluated the sperm parameters such as cauda epididymis weight, sperm count, sperm morphology and sperm DNA stability of adult CF-1 male mice treated daily (oral exposure) with the toxic sodium arsenite (As, 7.0 mg/kg/body weight); Melatonin (Me, 10.0 mg/kg/bw), Me (10.0 mg/kg/bw) plus As (7.0 mg/kg/bw) and Negative Control (NaCl 0.9%) to assess acute (8.3 days), chronic (33.2 days) and recovery of testicular damage (66.4 days). Arsenic decreases the number of sperm from chronic treatment (33.2 days) and this effect continued until 66.4 days of treatment. The toxic effect of As also altered the morphology of spermatozoa in all treatment periods when compared to the negative control group. However, Metalonin induced protective effects in periods of 33.2 and 66.4 days of treatment. Additionally, the stability of DNA was significantly affected by arsenic in all periods, but the chronic treatment (33.2 days) in the AsMe revealed increased stability compared to the group treated with arsenic only. Melatonin partially protects sperm toxicity caused by Arsenic, especially during periods of 33.2 and 66.4 days. 1252In this work, we aim to determine the effects of acute, chronic and recovery of testicular exposure to sodium arsenite in epididymal sperm and assess the use of melatonin as a protective agent and antioxidant. MATERIAL AND METHODThree-month-old male mice (Mus musculus) strain CF-1, healthy and sexually mature, were obtained from the Faculty of Medicine, University of Chile. The animals were maintained in a room under controlled conditions of temperature (22±2°C), and a 12 h light/dark cycle, with ad libitum access to commercial pellets and tap water.Reproductive changes were studied as acute (8.3 days), chronic (33.2 days) and recovery of testicular damage (66.4 days) in 88 adult mice exposed every day to oral doses of Sodium Arsenite (As; 7.0 mg/kg/bw, Sigma Chemical Co., St. Louis, MO); Melatonin (Me; 10.0 mg/kg/bw, Arama Laboratorios SA, Santiago, Chile) (Gutelkin et al., 2001); Me (10.0 mg/kg/bw) plus As (7.0 mg/kg/bw), and Negative Control (NaCl 0.9%) delivered orally in a volume not greater than 0.05 mL.Before the beginning and after the end of treatment, all animals were weighted. Euthanasia was performed by cervical dislocation after anesthesia with ketamine (Laboratory Biosano SA, Santiago, Chile) according to the protocol of animal handling of the Bioethics Committee of the Faculty of Medicine, University of Chile. Sperm Parameters.Extraction, weighing and sperm count in epididymalcauda. After obtaining the cauda epididymis they were weighed. Then sperm suspension was obtained using the protocol by Fornés & Bustos-Obregón (1994). Sperm were counted at 200X in a microscope, equipped to use Makler® chamber, adding a drop of sperm suspension by capillary and counting in duplicate the sperm present in the 100 squares of the camera, expressing this result as a million sperm/mg epididymis. Sperm morphology analysis.From the sperm suspension obtained above it was obtained 200 µL of sample. Addit...

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Section: Discussionmentioning

confidence: 99%

Melatonin Protective Role in Mouse Cauda Epipidymal Spermatozoa Damage Induced by Sodium Arsenite

et al. 2013

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“…The reaction between an antioxidant and DPPH reflects the ability of the antioxidant to donate its hydrogen to DPPH [Musialik and Litwinienko, 2005]. The antioxidative activities of some tricyclic aromatic amines and melatonin reacting with ABTS þ: and DPPH have been determined [Zhao et al, 2008;Tang and Liu, 2007a]. Whether the N-H in DaH also reacts with ABTS þ: and DPPH can provide direct evidence for radical trapping activity of DaH.…”

Section: And Dpphmentioning

confidence: 98%

“…DaH may induce nephrotoxicity in vivo and is involved in oxidative stress-mediated genomic DNA fragmentation and apoptosis [Hickey et al, 2001]. Comparison of the free-radical-scavenging activity of DaH with its sodium salt in AAPH-induced hemolysis of human erythrocytes [Tang and Liu, 2006] showed that melatonin, an antioxidant can protect DNA against AAPH-induced oxidative damage [Zhao et al, 2008]. This led to the present study investigating whether DaH has antioxidant properties and may potentially protect DNA against AAPH-induced oxidative damage, in which TBARS is measured to quantitate the oxidative degree of DNA.…”

Section: à5mentioning

confidence: 99%

“…However, no t inh is generated when trolox or a-tocopherol is used to protect DNA against AAPHinduced oxidative damage, such that R i cannot be obtained. The rate of radical generation (R g ) is equal to that of the radical initiation (R i ) in AAPH-induced erythrocyte hemolysis viz., R i 5 R g 5 (8.471.2) Â 10 À5 Â 40 mM Á min À1 5 3.36 mM Á min À1 [Tang and Liu, 2007b], assuming that R i 5 R g is still available for AAPH-induced oxidative damage of DNA to calculate n in this case [Zhao et al, 2008]. Thus, the n-value of DaH (n DaH ) and its sodium salt (n DaNaH ) can be obtained by the multiple between the coefficient in Equations 1 and 2 and R g , resulting in n DaH 5 3.86 (70.54) and n DaNaH 5 3.56 (70.54).…”

Section: Antioxidant Effects Of Dah and Its Sodium Saltmentioning

confidence: 99%

“…AAPH-induced oxidative damage of DNA was performed as described [Zhao et al, 2008]. DaH was dissolved in dimethylsulfoxide (DMSO), and its sodium salt in PBS.…”

Section: Aaph-induced Oxidative Damagementioning

confidence: 99%

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Diclofenac acid: a free‐radical‐scavenger to protect DNA against radical‐induced oxidation

Tang

Liu

2009

Drug Development Research

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The present work focused on the antioxidant effects of diclofenac acid (DaH) and its sodium salt (DaNaH) on the radical-induced oxidation of DNA. 2,2 0 -Azobis(2-amidinopropane) dihydrochloride (AAPH) was used as radical initiator to oxidize naked DNA sodium salt, followed by the determination of thiobarbituric acid reactive substance (TBARS). DaH and DaNaH also interacted with two other radicals: 2,2 0 -azinobis(3-ethylbenzothiazoline-6-sulfonate) radical cation (ABTS þ: ) and 2,2 0 -diphenyl-1-picrylhydrazyl (DPPH). DaH and DaNaH produce a concentration-dependent protection of DNA. Kinetic studies established that either DaH or DaNaH trap 3-4 radicals when they protect DNA against AAPH-induced oxidation. DaH and DaNaH scavenged ABTS þ: efficiently. Diclofenac was thus found to be an antioxidant that concentration-dependently reduced radicals rather than donated its hydrogen atom to radicals. Drug Dev Res 70 : 520-524, 2009.

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Lidocaine: An inhibitor in the free‐radical‐induced hemolysis of erythrocytes

Tang

Liu

2009

J Biochem & Molecular Tox

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Lidocaine was reported to protect erythrocytes from hemolysis induced by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH). Since AAPH-induced hemolysis was a convenient in vitro experimental system to mimic erythrocytes undergoing peroxyl radicals attack, the aim of this work was to investigate the antioxidant effect of lidocaine on AAPH-induced hemolysis by chemical kinetics. As a result, one molecule of lidocaine can only trap 0.37 radical, much lower than melatonin. Meanwhile, lidocaine cannot protect erythrocytes from hemolysis induced by hemin, which the mechanism of hemolysis was due to the erythrocyte membrane destroyed by hemin. Accordingly, lidocaine protected erythrocytes by scavenging radicals preferentially rather than by stabilizing membrane. Moreover, the interactions of lidocaine with two radical species, including 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonate) radical cation (ABTS(+*)) and 2,2'-diphenyl-1-picrylhydrazyl (DPPH), indicated that lidocaine can reduce ABTS(+*) with 260 microM as the 50% inhibition concentration (IC(50)) and cannot react with DPPH. Thus, lidocaine served as a reductant rather than a hydrogen donor to interact with radicals. Finally, the quantum calculation proved that, compared with the melatonin radical, the stabilization of N-centered radical of lidocaine was higher than the amide-type N-centered radical but lower than the indole-type N-centered radical in melatonin. These results provided basic information for lidocaine to be an antiradical drug.

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Antioxidative effect of melatonin on DNA and erythrocytes against free-radical-induced oxidation

Cited by 39 publications

References 39 publications

Melatonin Protective Role in Mouse Cauda Epipidymal Spermatozoa Damage Induced by Sodium Arsenite

Melatonin Protective Role in Mouse Cauda Epipidymal Spermatozoa Damage Induced by Sodium Arsenite

Diclofenac acid: a free‐radical‐scavenger to protect DNA against radical‐induced oxidation

Lidocaine: An inhibitor in the free‐radical‐induced hemolysis of erythrocytes

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