Differential effects of quercetin and silymarin on arsenite-induced cytotoxicity in two human breast adenocarcinoma cell lines

Soria, Elio Andrés; Eynard, Aldo R.; Quiroga, Patricia; Bongiovanni, Guillermina A.

doi:10.1016/j.lfs.2007.09.008

Cited by 24 publications

(12 citation statements)

References 31 publications

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“…Unexpectedly, co-treatment with these compounds neutralised this effect, perhaps because it may depend on pharmacological interactions, though reciprocal chelation cannot be discarded (Mishra and Flora 2008). Such interactions are supported by our previous results about stress markers, which revealed different effects for Q alone and for As + Q co-exposure Soria et al 2007), which led to alterations in effectiveness and/or half-life, with different structure-dependent effects being found for Q and S (Tsujimoto et al 2009). Indeed, S exhibited antioxidant activity against the As-induced AHP increase without modifying the redox state of cells when it was administered alone.…”

Section: Discussionsupporting

confidence: 62%

Cytoprotective effects of silymarin on epithelial cells against arsenic-induced apoptosis in contrast with quercetin cytotoxicity

2010

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Section: Discussionsupporting

confidence: 62%

Cytoprotective effects of silymarin on epithelial cells against arsenic-induced apoptosis in contrast with quercetin cytotoxicity

2010

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“…4. Doses used were selected based on previous experiments and published literature [61]. All biochemical studies were performed at day 40 (before the start of PUFAs treatment) designed as breastfeeding weaning period, it was previously suggested that both obesity and type 2 DM may have their origins in the perinatal period, and at the end of 6 and 12 months of age [62, 63].…”

Section: Methodsmentioning

confidence: 99%

Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)

et al. 2016

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BackgroundDiabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed the effects of supplementation of ω-3 and ω-6 polyunsaturated fatty acids (PUFAs) with or without nordihydroguaiaretic acid (NDGA) added, an antioxidant and lipoxygenase inhibitor, on metabolic and inflammatory parameters in eSS rats to evaluate whether they can delay development and/or prevent progression of DM.MethodsAfter weaning, eSS rats received, intraperitoneally, once a month ω-3 (EPA 35% and DHA 40%–6.25 mg/Kg) or ω-6 (90% arachidonic acid- 6. 25 mg/Kg) for twelve months. Two additional groups of rats received 1.9 mg/kg NDGA added to ω-3 and ω-6 fatty acids. Blood samples were collected at day 40, and at the end of the 6th month and 12th month of age to determine plasma triglycerides (TGs), total plasma fatty acids (FA), A1C hemoglobin (HbA1C), C-reactive protein (CRP), gamma glutamyl transpeptidase (GGT), lipo and hydro peroxides, nitrites and IL-6 (in plasma and liver, kidney, and pancreas) and underwent oral glucose tolerance test (OGTT) as well. Wistar and eSS rats that received saline solution were used as controls.ResultsPlasma lipids profile, TG, fasting and post-prandial blood glucose levels, and glycosylated HbA1C showed significant improvements in ω-3 and ω-3 + NDGA treated animals compared to eSS control group. ω-3 and ω-3 + NDGA groups showed an inverse correlation with fasting blood glucose and showed lower plasma levels of GGT, TG, and CRP. eSS rats treated with ω-3 LCPUFAs showed reduced level of inflammatory and oxidative indices in plasma and liver, kidney and pancreas tissues in comparison with eSS control (non-treated) and ω-6 treated groups.ConclusionseSS rats are a useful model to study type 2 DM pathophysiology and related inflammatory indices. ω-3 + NDGA supplementation, at the doses tested, ameliorated inflammatory, metabolic and oxidative stress markers studied.

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“…Besides, As can react with protein and nonprotein thiol groups, leading to the alteration of signaling pathways, structural modifications, and enzyme inactivation [6], which may stimulate reactive oxygen species (ROS) production [5]. Oxidative stress is recognized as a possible mechanism implicated in both As-induced apoptosis and carcinogenicity [7,8]. The resistance to As toxicity in mammalian cells is correlated with higher levels of reduced glutathione (GSH) and GSH-related enzymes [5,6].…”

Section: Introductionmentioning

confidence: 99%

Acute toxicity of arsenic and oxidative stress responses in the embryonic development of the common South American toad Rhinella arenarum

Mardirosian

Lascano

Ferrari³

et al. 2015

Enviro Toxic and Chemistry

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Arsenic (As), a natural element of ecological relevance, is found in natural water sources throughout Argentina in concentrations between 0.01 mg/L and 15 mg/L. The autochthonous toad Rhinella arenarum was selected to study the acute toxicity of As and the biochemical responses elicited by the exposure to As in water during its embryonic development. The median lethal concentration (LC50) value averaged 24.3 mg/L As and remained constant along the embryonic development. However, As toxicity drastically decreased when embryos were exposed from heartbeat-stage on day 4 of development, suggesting the onset of detoxification mechanisms. Given the environmental concentrations of As in Argentina, there is a probability of exceeding lethal levels at 1% of sites. Arsenic at sublethal concentrations caused a significant decrease in the total antioxidant potential but generated an increase in endogenous glutathione (GSH) content and glutathione S-transferase (GST) activity. This protective response might prevent a deeper decline in the antioxidant system and further oxidative damage. Alternatively, it might be linked to As conjugation with GSH for its excretion. The authors conclude that toad embryos are more sensitive to As during early developmental stages and that relatively high concentrations of this toxic element are required to elicit mortality, but oxidative stress may be an adverse effect at sublethal concentrations.

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Differential effects of quercetin and silymarin on arsenite-induced cytotoxicity in two human breast adenocarcinoma cell lines

Cited by 24 publications

References 31 publications

Cytoprotective effects of silymarin on epithelial cells against arsenic-induced apoptosis in contrast with quercetin cytotoxicity

Cytoprotective effects of silymarin on epithelial cells against arsenic-induced apoptosis in contrast with quercetin cytotoxicity

Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)

Acute toxicity of arsenic and oxidative stress responses in the embryonic development of the common South American toad Rhinella arenarum

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