The Role of Oxidative Stress in Hormesis Induced by Sodium Arsenite in Human Embryo Lung Fibroblast (HELF) Cellular Proliferation Model

Yang, Ping; He, Xiaoqing; Peng, Lei; Li, Aiping; Wang, Xinru; Zhou, Jianmin; Liu, Qi-Zhan

doi:10.1080/15287390701290832

Cited by 69 publications

(40 citation statements)

References 36 publications

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“…At low levels, ROS modulate gene expression by acting as second messengers, but at high levels they cause oxidative injury leading to cell death (13,15). We hypothesized that the CaA-induced improvement of cell viability and protection against DNA damage following H 2 O 2 treatment were mediated by the generation of low levels of ROS.…”

Section: Resultsmentioning

confidence: 99%

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Caffeic acid improves cell viability and protects against DNA damage: involvement of reactive oxygen species and extracellular signal-regulated kinase

Chen

Jiang

et al. 2015

Braz J Med Biol Res

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Hormesis is an adaptive response to a variety of oxidative stresses that renders cells resistant to harmful doses of stressing agents. Caffeic acid (CaA) is an important antioxidant that has protective effects against DNA damage caused by reactive oxygen species (ROS). However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved. We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs). In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role. CaA also activated the extracellular signal-regulated kinase (ERK) signal pathway in a time-dependent manner. Inhibition of ERK by its inhibitor U0126 or by its specific small interfering RNA (siRNA) blocked the CaA-induced improvement in cell viability and the protective effects against H2O2-mediated DNA damage. This study adds to the understanding of the antioxidant effects of CaA by identifying a novel molecular mechanism of enhanced cell viability and protection against DNA damage.

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Section: Resultsmentioning

confidence: 99%

“…It has long been recognized that ROS cause complex and irreversible damage to cellular constituents that impairs cellular homeostasis (15). Oxidative damage is related to the high reactivity of molecular oxygen and its intermediates, which can lead to oxidative modifications of proteins, lipids, and DNA (15).…”

Section: Discussionmentioning

confidence: 99%

Caffeic acid improves cell viability and protects against DNA damage: involvement of reactive oxygen species and extracellular signal-regulated kinase

Chen

Jiang

et al. 2015

Braz J Med Biol Res

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“…Various reports indicate that the generation of ROS, oxidative stress and cellular damage through lipid peroxidation is the major pathway for the pathogenesis of sodium arsenite [6,7]. It has been reported that intracellular ROS levels produced is dependent on the concentration of sodium arsenite which further determine the type and severity of biological/pathological effects [8].…”

Section: Introductionmentioning

confidence: 99%

Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway

et al. 2017

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(2017) Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway, Redox Report, 22:6, 467-477, DOI: 10.1080/13510002.2017 Objectives: Arsenic is a ubiquitous element that is widely distributed in the environment to which man and animals are exposed. Cardiovascular disease is one of the aftermaths of chronic arsenic exposure-related morbidity and mortality. This study sought to investigate the possibility of reversal from arsenic-induced cardio-renal toxicity following exposure and subsequent withdrawal. The study also seeks to understand the mechanism of action of this reversal. Methods: Rats were orally exposed to sodium arsenite at 10, 20 and 40 mg/kg daily for 4 weeks followed by 4 weeks of withdrawal. Results: Exposure to arsenic caused a significant increase in malondialdehyde, H 2 O 2 generation but decrease total thiol and reduced glutathione levels in both cardiac and renal tissues. Furthermore, increases in superoxide dismutase, glutathione-S-transferase and catalase with significant increases in glutathione peroxidase activities were observed in the cardiac tissues. On the contrary, a significant reduction in the renal antioxidant enzyme activity was recorded following exposure. Also, antioxidant defense system did not return to apparent values after arsenic withdrawal. Immunohistochemistry revealed a reduction in the expression of the prosurvival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.

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“…Determination of dose-response effects is general procedure in toxicology for risk evaluation and the establishment of exposure guidelines in view of monophasic responses. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay has been widely used toward this end and has also permitted to reveal in some cases biphasic hormesis responses (13,14,43,51). Hormesis has been defined as a dose-response relationship in which a stimulatory response occurs at low doses, and an inhibitory response takes place at high doses, resulting in a U-or inverted U-shaped dose response (10).…”

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confidence: 99%

Characterization of oxidized low-density lipoprotein-induced hormesis-like effects in osteoblastic cells

Hamel¹,

Abed²,

Brissette³

et al. 2008

American Journal of Physiology-Cell Physiology

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Hamel P, Abed E, Brissette L, Moreau R. Characterization of oxidized low-density lipoprotein-induced hormesis-like effects in osteoblastic cells. Am J Physiol Cell Physiol 294: C1021-C1033, 2008. First published February 20, 2008 doi:10.1152/ajpcell.00361.2007.-Epidemiological studies indicate that patients suffering from atherosclerosis are predisposed to develop osteoporosis. Atherogenic determinants such as oxidized low-density lipoprotein (oxLDL) particles have been shown both to stimulate the proliferation and promote apoptosis of bone-forming osteoblasts. Given such opposite responses, we characterized the oxLDL-induced hormesis-like effects in osteoblasts. Biphasic 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reductive activity responses were induced by oxLDL where low concentrations (10 -50 g/ml) increased and high concentrations (from 150 g/ml) reduced the MTT activity. Cell proliferation stimulation by oxLDL partially accounted for the increased MTT activity. No alteration of mitochondria mass was noticed, whereas low concentrations of oxLDL induced mitochondria hyperpolarization and increased the cellular levels of reactive oxygen species (ROS). The oxLDL-induced MTT activity was not related to intracellular ROS levels. OxLDL increased NAD(P)H-associated cellular fluorescence and flavoenzyme inhibitor diphenyleneiodonium reduced basal and oxLDL-induced MTT activity, suggesting an enhancement of NAD(P)H-dependent cellular reduction potential. Low concentrations of oxLDL reduced cellular thiol content and increased metallothionein expression, suggesting the induction of compensatory mechanisms for the maintenance of cell redox state. These concentrations of oxLDL reduced osteoblast alkaline phosphatase activity and cell migration. Our results indicate that oxLDL particles cause hormesis-like response with the stimulation of both proliferation and cellular NAD(P)H-dependent reduction potential by low concentrations, whereas high concentrations lead to reduction of MTT activity associated with the cell death. Given the effects of low concentrations of oxLDL on osteoblast functions, oxLDL may contribute to the impairment of bone remodeling equilibrium.osteoblasts; atherosclerosis; oxysterol ELEVATED LEVELS of serum low-density lipoprotein (LDL) particles are considered as the most important atherogenic risk factor. LDL particles are thought to become atherogenic after undergoing oxidative modifications, and key roles of oxidized LDL (various oxidized species collectively designated oxLDL) in atherosclerosis have been largely reviewed by Steinberg (46). OxLDL and oxysterols have been shown to increase or decrease proliferation and trigger the apoptosis process depending on the cell types related to vasculature alterations, nature of oxLDL and oxysterols, and on the concentrations used (52), thus supporting numerous deleterious effects that sustain the development of atherosclerosis. Also, a number of clinical studies suggest an association between cardiovascular disease and the develo...

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The Role of Oxidative Stress in Hormesis Induced by Sodium Arsenite in Human Embryo Lung Fibroblast (HELF) Cellular Proliferation Model

Cited by 69 publications

References 36 publications

Caffeic acid improves cell viability and protects against DNA damage: involvement of reactive oxygen species and extracellular signal-regulated kinase

Caffeic acid improves cell viability and protects against DNA damage: involvement of reactive oxygen species and extracellular signal-regulated kinase

Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway

Characterization of oxidized low-density lipoprotein-induced hormesis-like effects in osteoblastic cells

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