Ameliorative effect of diallyl trisulphide on arsenic-induced oxidative stress in rat erythrocytes and DNA damage in lymphocytes

Prabu, S. Milton; Sumedha, Naorem Chanu

doi:10.1515/jbcpp-2013-0047

Cited by 21 publications

(7 citation statements)

References 26 publications

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“…Diallyl trisulfide demonstrates antioxidative effects, which are associated with the changes in the activity of antioxidant enzymes and the level of glutathione (Wu et al 2004 ; Zhang et al 2016 ; Zeng et al 2008 ; Mostafa et al 2016 ; Prabu and Sumedha 2014 ; Hu et al 2007 ).…”

Section: Introductionmentioning

confidence: 99%

A possible mechanism of inhibition of U87MG and SH-SY5Y cancer cell proliferation by diallyl trisulfide and other aspects of its activity

et al. 2017

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The study was conducted to elucidate the mechanism of antiproliferative and antioxidative action of diallyl trisulfide (DATS), a garlic-derived organosulfur compound. Changes in the l-cysteine desulfuration, and the levels of cystathionine and non-protein thiols in DATS-treated human glioblastoma (U87MG) and neuroblastoma (SH-SY5Y) cells were investigated. The inhibition of proliferation of the investigated cells by DATS was correlated with an increase in the inactivated form of Bcl-2. In U87MG cells, an increased level of sulfane sulfur and an increased activity of 3-mercaptopyruvate sulfurtransferase (MPST) and rhodanese, the enzymes involved in sulfane sulfur generation and transfer, suggest that DATS can function as a donor of sulfane sulfur atom, transferred by sulfurtransferases, to sulfhydryl groups of cysteine residues of Bcl-2 and in this way lower the level of active form of Bcl-2 by S-sulfuration. Diallyl trisulfide antioxidative effects result from an increased level of cystathionine, a precursor of cysteine, and an increased glutathione level. MPST and rhodanese, the level of which is increased in the presence of DATS, can serve as antioxidant proteins.

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Section: Introductionmentioning

confidence: 99%

A possible mechanism of inhibition of U87MG and SH-SY5Y cancer cell proliferation by diallyl trisulfide and other aspects of its activity

et al. 2017

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“…The leaf, fruit, and seed extracts of this plant contain phenolic antioxidant compounds such as quercetin and kaempferol [133][134][135]. Diallyl trisulfide (DATS), an organosulfur compound from garlic (Allium sativum) oil, has been found protective against arsenic-induced genotoxicity in rat lymphocytes, and this protection was associated with reduced oxidative stress [136]. The effects of different antioxidants on arsenic genotoxicity are summarized in Table 1.…”

Section: Role Of Antioxidants In Combating Arsenic Genotoxicitymentioning

confidence: 99%

“…MDA has been identified to bind to DNA and to damage it [150]. Antioxidant administrations in arsenicintoxicated animals have resulted in decreased lipid peroxidation as well as reduced DNA damage [121,122,136]. δ-Aminolevulinic acid dehydratase (ALAD) is a sulfhydryl-containing enzyme, and it plays a key role in heme biosynthesis pathway [151].…”

Section: Protective Mechanism Of Antioxidants Against Arsenic Genotoxmentioning

confidence: 99%

“…↓ DNA migration in comet assay [136] ↓=decrease BW body weight, NaAsO 2 sodium arsenite, As 2 O 3 arsenic trioxide ALAD activity in arsenic-intoxicated animals supplemented with antioxidants [59, 125]. Antioxidant administration in arsenic-intoxicated animals has resulted in decreased arsenic concentration in different organs of the body, particularly the liver, kidney, blood, and brain [154,155].…”

Section: Protective Mechanism Of Antioxidants Against Arsenic Genotoxmentioning

confidence: 99%

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Natural Antioxidants Against Arsenic-Induced Genotoxicity

Kumar

Lalit

Thakur

2015

Biol Trace Elem Res

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Arsenic is present in water, soil, and air in organic as well as in inorganic forms. However, inorganic arsenic is more toxic than organic and can cause many diseases including cancers in humans. Its genotoxic effect is considered as one of its carcinogenic actions. Arsenic can cause DNA strand breaks, deletion mutations, micronuclei formation, DNA-protein cross-linking, sister chromatid exchange, and DNA repair inhibition. Evidences indicate that arsenic causes DNA damage by generation of reactive free radicals. Nutritional supplementation of antioxidants has been proven highly beneficial against arsenic genotoxicity in experimental animals. Recent studies suggest that antioxidants protect mainly by reducing excess free radicals via restoring the activities of cellular enzymatic as well as non-enzymatic antioxidants and decreasing the oxidation processes such as lipid peroxidation and protein oxidation. The purpose of this review is to summarize the recent literature on arsenic-induced genotoxicity and its mitigation by naturally derived antioxidants in various biological systems.

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“…Furthermore, these changes were accompanied by decreased SOD and increased catalase activities. Recently, Prabu and Sumedha [30] demonstrated that rats orally administered with 5 mg/kg of arsenic for 28 days showed significant alterations in plasma marker enzymes, plasma and erythrocyte membrane oxidative stress markers, erythrocyte membrane antioxidant enzymes, and non-antioxidant enzymes indicative of oxidative stress in erythrocytes. Arsenic exposure also reduced the activity of membrane bound ATPase and increased the percentage of DNA tail length in lymphocytes, suggesting DNA damage.…”

Section: Erythrocytesmentioning

confidence: 99%