Comparative effects of cadmium, copper, paraquat and benzo[a]pyrene on the actin cytoskeleton and production of reactive oxygen species (ROS) in mussel haemocytes

Gómez-Mendikute, Amagoia; Cajaraville, Miren P.

doi:10.1016/s0887-2333(03)00093-6

Cited by 163 publications

(66 citation statements)

References 36 publications

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“…Previous studies have reported various results about the heavy metal toxicity on mollusks. For example, cadmium/copper caused no change in ROS production in mussel (Goméz-Mandikute and Cajaraville 2003). But sodium arsenite could inhibit the activities of CAT and induce oxidative stress in the gills of Lamellidens marginalis (Chakraborty et al 2010).…”

Section: Discussionmentioning

confidence: 95%

Effects of heavy metals on the expression of a zinc-inducible metallothionein-III gene and antioxidant enzyme activities in Crassostrea gigas

Cong

Liu

et al. 2012

Ecotoxicology

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Sequestration by metallothioneins and antioxidant defense are two kinds of important defense mechanisms employed by mollusks to minimize adverse effects caused by heavy metal contaminants in marine environment. In the present study, a novel metallothionein gene, CgMT-III, was cloned from Crassostrea gigas, consisting of eighteen conserved cysteine residues and encoding a MT III-like protein with two tandem b domains. The expression level of CgMT-III transcript induced by zinc was much higher than that induced by cadmium exposure. It suggested that CgMT-III was perhaps mainly involved in homeostatic control of zinc metabolism, which was distinct from previously identified MTs in C. gigas. Among the tested antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), SOD and GPx showed varying up-regulations in a tissuespecific manner, while CAT activities were inhibited in both gill and hepatopancreas from C. gigas exposed to heavy metals. It can be inferred that CgMT-III was mainly involved in zinc homeostasis, and CgMT-III gene together with CAT enzyme could be potential biomarkers to indicate heavy metal, especially zinc pollution in marine organisms.

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Section: Discussionmentioning

confidence: 95%

Effects of heavy metals on the expression of a zinc-inducible metallothionein-III gene and antioxidant enzyme activities in Crassostrea gigas

Cong

Liu

et al. 2012

Ecotoxicology

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“…Environmental pollution is a major cause of concern as numerous pollutants are known to be involved in a variety of diseases in humans [1]. Elevated levels of bioavailable metals have been implicated in cancers, neurological complications, pulmonary diseases and nephrological abnormalities [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Aluminum-Induced Mitochondrial Dysfunction Leads to Lipid Accumulation in Human Hepatocytes: A Link to Obesity

Mailloux¹,

Lemire²,

Appanna³

2007

Cell Physiol Biochem

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Mitochondrial dysfunction is the cause of a variety of pathologies associated with high energy-requiring tissues like the brain and muscles. Here we show that aluminum (Al) perturbs oxidative-ATP production in human hepatocytes (HepG2 cells). This Al-induced mitochondrial dysfunction promotes enhanced lipogenesis and the accumulation of the very low density lipoprotein (VLDL). Al-stressed HepG2 cells secreted more cholesterol, lipids and proteins than control cells. The level of apolipoprotein B-100 (ApoB-100) was markedly increased in the culture medium of the cells exposed to Al. ¹³C-NMR and HPLC studies revealed a metabolic profile favouring lipid production and lowered ATP synthesis in Al-treated cells. Electrophoretic and immunoblot analyses pointed to increased activities and expression of lipogenic enzymes such as glycerol 3-phosphate dehydrogenase (G3PDH), acetyl CoA carboxylase (ACC) and ATP-citrate lyase (CL) in the hepatocytes exposed to Al, and a sharp diminution of enzymes mediating oxidative phosphorylation. D-Fructose elicited the maximal secretion of VLDL in the Al-challenged cells. These results suggest that the Al-evoked metabolic shift favours the accumulation of lipids at the expense of oxidative energy production in hepatocytes.

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“…The intracellular ROS generation is a crucial mediator to trigger cytoskeleton reorganization and endothelial hyperpermeability [14,15]. Thus, we investigated whether SalA function as an effective anti-oxidant in endothelial cells after IS/RP.…”

Section: Resultsmentioning

confidence: 99%

SalA Attenuates Ischemia/Reperfusion-Induced Endothelial Barrier Dysfunction via Down-Regulation of VLDL Receptor Expression

Yang

Zhang

Wang³

et al. 2014

Cell Physiol Biochem

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Background: Salvianolic acid A (SalA) has been shown to confer robust protection against endothelial injury. VLDL receptor is expressed at high levels on the endothelial surface, however its biological effect on endothelial cells has not yet been completely elucidated. Here, we investigated molecular effects of SalA on endothelial VLDL expression and barrier dysfunction under conditions of ischemia/reperfusion (IS/RP). Methods: Human umbilical vein endothelial cells (HUVECs) treated with SalA were subjected to IS/RP stimulation. Endothelial permeability, ZO-1 distribution, actin cytoskeleton reorganization, and intracellular reactive oxygen species (ROS) generation were examined. The mRNA levels were tested by real-time RT-PCR and the protein levels were determined by immunoblot analysis. Results: Pretreatment of HUVECs with SalA markedly attenuated IS/RP-induced endothelial hyperpermeability, discontinuous ZO-1 staining, actin stress fiber formation, and intracellular ROS generation. IS/RP activated p38 MAPK signaling and enhanced VLDL receptor expression, and inactivation of p38 MAPK abolished increase of VLDL receptor expression. Furthermore, siRNA experiments showed that VLDL receptor was a crucial mediator of endothelial barrier dysfunction and intracellular ROS generation induced by IS/RP. Importantly, SalA effectively suppressed IS/RP-induced activation of p38 MAPK signaling and increase of VLDL receptor expression. Conclusion: These results for the first time demonstrated that SalA protected against IS/RP-induced endothelial barrier dysfunction through suppression of VLDL receptor expression.

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Comparative effects of cadmium, copper, paraquat and benzo[a]pyrene on the actin cytoskeleton and production of reactive oxygen species (ROS) in mussel haemocytes

Cited by 163 publications

References 36 publications

Effects of heavy metals on the expression of a zinc-inducible metallothionein-III gene and antioxidant enzyme activities in Crassostrea gigas

Effects of heavy metals on the expression of a zinc-inducible metallothionein-III gene and antioxidant enzyme activities in Crassostrea gigas

Aluminum-Induced Mitochondrial Dysfunction Leads to Lipid Accumulation in Human Hepatocytes: A Link to Obesity

SalA Attenuates Ischemia/Reperfusion-Induced Endothelial Barrier Dysfunction via Down-Regulation of VLDL Receptor Expression

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