Carcinogenic metal induced sites of reactive oxygen species formation in hepatocytes

Pourahmad, Jalal; O’Brien, Peter J.; Jokar, Farzaneh; Daraei, Bahram

doi:10.1016/s0887-2333(03)00123-1

Cited by 148 publications

(88 citation statements)

References 19 publications

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“…3). It should also be noted that, apparently, the results reported here seem to be in contrast with a previous paper stating that the targets of Co 2+ to produce ROS are lysosomes instead of mitochondria, as ATP glycolytic generators cannot prevent oxidative stress in hepatocytes (Pourahmad et al, 2003). The results reported here do not exclude the participation of lysosomes in oxidative stress leading to apoptosis, but the involvement of mitochondria is unequivocally proven.…”

Section: Discussioncontrasting

confidence: 99%

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Cobalt induces oxidative stress in isolated liver mitochondria responsible for permeability transition and intrinsic apoptosis in hepatocyte primary cultures

Battaglia

Compagnone

Bandino

et al. 2009

The International Journal of Biochemistry & Cell Biology

102

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a b s t r a c tIt is well established that cobalt mediates the occurrence of oxidative stress which contributes to cell toxicity and death. However, the mechanisms of these effects are not fully understood. This investigation aimed at establishing if cobalt acts as an inducer of mitochondrial-mediated apoptosis and at clarifying the mechanism of this process.Cobalt, in the ionized species Co 2+ , is able to induce the phenomenon of mitochondrial permeability transition (MPT) in rat liver mitochondria (RLM) with the opening of the transition pore. In fact, Co 2+ induces mitochondrial swelling, which is prevented by cyclosporin A and other typical MPT inhibitors such as Ca 2+ transport inhibitors and bongkrekic acid, as well as anti-oxidant agents. In parallel with mitochondrial swelling, Co 2+ also induces the collapse of electrical membrane potential. However in this case, cyclosporine A and the other MPT inhibitors (except ruthenium red and EGTA) only partially prevent « drop, suggesting that Co 2+ also has a proton leakage effect on the inner mitochondrial membrane. MPT induction is due to oxidative stress, as a result of generation by Co 2+ of the highly damaging hydroxyl radical, with the oxidation of sulfhydryl groups, glutathione and pyridine nucleotides. Co 2+ also induces the release of the pro-apoptotic factors, cytochrome c and AIF. Incubation of rat hepatocyte primary cultures with Co 2+ results in apoptosis induction with caspase activation and increased level of expression of HIF-1␣.All these observations allow us to state that, in the presence of calcium, Co 2+ is an inducer of apoptosis triggered by mitochondrial oxidative stress.

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Section: Discussioncontrasting

confidence: 99%

“…The possibility that Co 2+ can induce oxidative stress in hepatocytes by increasing the formation of ROS, with the results of provoking cell death has been examined also by other authors (Pourahmad et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Cobalt induces oxidative stress in isolated liver mitochondria responsible for permeability transition and intrinsic apoptosis in hepatocyte primary cultures

Battaglia

Compagnone

Bandino

et al. 2009

The International Journal of Biochemistry & Cell Biology

102

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“…The reaction was performed by mixing the diluted supernatant, phosphate EDTA buffer (pH 8.3), and OPT (50 μg/mL) solution, and the mixture was incubated at 37℃ in darkness for 15 min. The fluorescence was read at an emission wavelength of 420 nm and an excitation wavelength of Lysosomal membrane stability assay Lysosomal membrane stability was determined with a modified method (Pourahmad et al, 2003). After being treated with 6-gingerol (10, 20, 40 μM) for 24 h, and adding hydrogen peroxide (50 μM) for 1 h, the cells were washed twice with PBS and incubated with acridine orange (AO)…”

Section: ×10mentioning

confidence: 99%

“…NAC ( Mitochondrial membrane potential assay Mitochondrial membrane potential was measured using amodified method (Pourahmad et al, 2003). Rhodamine 123 was used for the estimation of mitochondrial membrane potential.…”

Section: ×10mentioning

confidence: 99%

6-Gingerol Attenuates Hydrogen Peroxide-induced DNA Damage in Human Umbilical Vein Endothelia Cells

Wang

Yang

Jiang

et al. 2014

FSTR

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An imbalance of oxidation and antioxidation is one of the primary causes of atherosclerosis. The use of naturalplant compounds with effects has been proven to have clinical relevance. 6-Gingerol, one of the major components of ginger, has diverse pharmacologic effects. In this study, the chemoprotective effect of 6-gingerol against hydrogen peroxide-induced DNA damage in human umbilical vein endothelia cells (HUVECs) was investigated. The comet assay was used to monitor DNA strand breaks. To further elucidate the underlying mechanisms, we tested lysosomal membrane stability, mitochondrial membrane potential, the intracellular generation of reactive oxygen species (ROS) and reduced glutathione (GSH). Our data revealed that 6-gingerol significantly reduced the DNA strand breaks caused by hydrogen peroxide. 6-Gingerol effectively suppressed hydrogen peroxide-induced intracellular ROS formation. The GSH depletion in HUVECs was also attenuated by 6-gingerol pretreatment. Moreover, lysosomal membrane stability was destroyed and mitochondrial membrane potential decreased after treated by hydrogen peroxide. Those effects can be protected by 6-gingerol. These firmly indicate 6-gingerol has a strong protective ability against the DNA damage caused by hydrogen peroxide in HUVECs, and the mechanism may relate to the antioxidant activity. Our data suggest 6-gingerol may be beneficial in the prevention of atherosclerosis.

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“…Several heavy metals can bind to sulphydrilic, aminic, and carboxylic groups of membrane proteins, so modifying membrane structure and permeability (Victery et al, 1984;HerakKramberger and Sabolic, 2001). Moreover they can induce oxidative stress (Koizumi et al, 1996;Pourahmad et al, 2003), cell proliferation and tumour production in renal tubules (Nolan and Shaikhu, 1992), necrosis and apoptosis with successive compensative regeneration (Tanimoto et al, 1993;Hamada et al, 1996;Bomhard et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Cell‐cycle protein modifications in the kidney of Mus spretus from Doñana National Park

Leoni

Torrice

Chiuchiarelli

et al. 2008

Environmental Toxicology

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On April 1998 a tailing dam of the Aznalcollar pyrite mine partially collapsed and released to the Guadiamar river acidic water and mud containing toxic metals threatening the Doñ ana National Park, a Spanish wildlife reserve located near the estuary of Guadalquivir river. To assess the possible biological effects on terrestrial ecosystems, biochemical markers were assayed in the kidneys of Algerian mice (Mus spretus) collected in several areas of Doñ ana and Guadiamar river. Biomarkers assayed are proteins involved in cell cycle regulation, in particular cyclins and their associated kinases, and some cell cycle inhibitors. Moreover Mitogen Activated Protein Kinases (MAPK), a signal transduction system involved in cell division, p53, a protein involved in growth arrest after DNA damage, and HSP70, an early stressinduced protein, were assayed. The kidneys of animals collected one year after the ecological disaster had increased levels of PCNA (proliferating cell nuclear antigen), indicating an increased number of cells in the S phase of cell cycle. This shift of cells from G0 to S phase is due to increased levels of cyclins D1, E, and A, to decreased levels of p21 and p27 cdk inhibitors, and to activation of MAPK cascade. On the other hand, p53 and HSP70 levels are not changed. These data demonstrate that the presence of toxic metals after ecological disaster provoked the induction of kidney cell proliferation interpretable as a compensatory cell growth after tissue damage and apoptosis, and that could lead to the genomic instability characteristic of cancer cell. # 2008 Wiley Periodicals, Inc. Environ Toxicol 23: 44-51, 2008

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Carcinogenic metal induced sites of reactive oxygen species formation in hepatocytes

Cited by 148 publications

References 19 publications

Cobalt induces oxidative stress in isolated liver mitochondria responsible for permeability transition and intrinsic apoptosis in hepatocyte primary cultures

Cobalt induces oxidative stress in isolated liver mitochondria responsible for permeability transition and intrinsic apoptosis in hepatocyte primary cultures

6-Gingerol Attenuates Hydrogen Peroxide-induced DNA Damage in Human Umbilical Vein Endothelia Cells

Cell‐cycle protein modifications in the kidney of Mus spretus from Doñana National Park

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