Inhibition of cadmium-induced apoptosis by glutathione S-transferase P1 via mitogen-activated protein kinases and mitochondrial pathways

Zhang, Chao; Yuan, Xianxian; Mao, Weiping; Yue, Ling; Kong, Xiuqin; Gao, Yanhong; Luo, Lan; Yin, Zhimin

doi:10.1016/j.etap.2010.06.004

Cited by 11 publications

(6 citation statements)

References 49 publications

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“…Furthermore, it has been reported that GSTP1 is involved in glutathione metabolism and could reduce excessive ROS and maintain redox balance [31]. Other studies showed that GSTP1 inhibited cell apoptosis through a mitochondrial and MAPK-associated pathway [32]. In summary, these results may provide a better understanding of the mechanism of the injury caused by S. agalactiae and the apoptosis of bMECs, which can be tested by further research.…”

Section: Discussionmentioning

confidence: 73%

Proteomic analysis of bovine mammary epithelial cells after in vitro incubation with S. agalactiae: potential biomarkers

Tong

Sun

Zhang

et al. 2020

Vet Res

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Streptococcus agalactiae is one of the causative agents of subclinical mastitis, a common disease of dairy cows that causes great economic losses in the industry worldwide. It is thought that pathology is mainly due to inflammatory damage of bovine mammary epithelial cells (bMECs); however, the mechanism by which S. agalactiae damages the bMECs is not clear. The aim of this study was to evaluate the inflammatory effects of S. agalactiae on bMECs and the resulting changes in protein profiles. The bMECs were incubated with S. agalactiae for different times and assayed for cell viability by MTT assay, apoptosis by annexin V and propidium iodide dual staining, and morphological and ultrastructural changes by scanning and transmission electron microscopy. Quantitative real-time PCR was used to determine the effect of S. agalactiae on expression of mRNA of inflammatory factors in bMECs and protein levels were quantitated by liquid chromatography/mass spectrometry. Exposure to S. agalactiae significantly decreased the cell viability and triggered apoptosis, as well as up-regulating TNF-α, IL-1β and IL-6 mRNA, and inhibiting IL-8 expression. S. agalactiae also induced morphological and ultrastructural changes. Furthermore, we identified 325 up-regulated and 704 down-regulated proteins in the treated vs control group. All significant differentially expressed proteins (DSEPs) were classified into three major areas by function: biological processes, cellular components and molecular functions. These differentially expressed proteins included enzymes and proteins associated with various metabolic processes and cellular immunity. Pathway enrichment analysis showed that eight down-regulated signaling pathways were significantly enriched. Exposure to even subclinical levels of S. agalactiae can lead to inflammation and bMEC damage. Our data suggest some possible molecular mechanisms for the harmful effects of subclinical mastitis in dairy cows.

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Section: Discussionmentioning

confidence: 73%

Proteomic analysis of bovine mammary epithelial cells after in vitro incubation with S. agalactiae: potential biomarkers

Tong

Sun

Zhang

et al. 2020

Vet Res

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“…Caspases (cysteine proteases), ceramides (cell membrane lipids), and calpains (Ca 2+dependent proteases) are known to play an important role in Cd 2+ -induced apoptosis in rat kidney proximal tubule cells and to be related directly to Cd 2+ -induced nephrotoxicity in vivo [191]. Cd 2+ induced apoptosis involving the activation of caspase-9, caspase-3 and mitogen-activated protein kinases (ERK, JNK, p53, and p38) as well as DNA fragmentation in rat C6 glioma cells, HEK293 cells, Vero cells, rat ascites hepatoma AS-30D cells, human lung cancer A549 cells, hamster ovary CHO-9 cells, PC12 cells, rat and mouse cochlea HEI-OC1 cells, rat primary astrocytes, rat primary cerebral cortical neurons, U-937 human promonocytic cells, mouse skin fibroblasts, NIH 3T3 cells, yeast cells, rat kidney proximal tubule cells, brain newborn rat oligodendrocytes, rat hepatocytes, mouse skin epidermal JB6 Cl41 cells, AS-30D ascites hepatoma cells, and human hepatocellular carcinoma HepG2 cells [146,158,159,161,162,172,[185][186][187]189,190,[192][193][194][195][196][197][198][199][200][201][202][203][204][205][206][207]. This Cd 2+ -induced apoptosis was accompanied by oxidative stress and mitochondrial injury, which manifested as a cell viability reduction, CI-CIII dysfunction, ATP depletion, ∆Ψ mito decline, matrix Ca 2+ load, a reduced glutathione decrease, cytochrome c release, an ROS and H 2 O 2 production increase, and lipid peroxidation as well as mitochondrial damage and swelling.…”

Section: Tl(i) Mitochondrial Researchmentioning

confidence: 99%

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Korotkov

2023

IJMS

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This review analyzes the causes and consequences of apoptosis resulting from oxidative stress that occurs in mitochondria and cells exposed to the toxic effects of different-valence heavy metals (Ag+, Tl+, Hg2+, Cd2+, Pb2+, Al3+, Ga3+, In3+, As3+, Sb3+, Cr6+, and U6+). The problems of the relationship between the integration of these toxic metals into molecular mechanisms with the subsequent development of pathophysiological processes and the appearance of diseases caused by the accumulation of these metals in the body are also addressed in this review. Such apoptosis is characterized by a reduction in cell viability, the activation of caspase-3 and caspase-9, the expression of pro-apoptotic genes (Bax and Bcl-2), and the activation of protein kinases (ERK, JNK, p53, and p38) by mitogens. Moreover, the oxidative stress manifests as the mitochondrial permeability transition pore (MPTP) opening, mitochondrial swelling, an increase in the production of reactive oxygen species (ROS) and H2O2, lipid peroxidation, cytochrome c release, a decline in the inner mitochondrial membrane potential (ΔΨmito), a decrease in ATP synthesis, and reduced glutathione and oxygen consumption as well as cytoplasm and matrix calcium overload due to Ca2+ release from the endoplasmic reticulum (ER). The apoptosis and respiratory dysfunction induced by these metals are discussed regarding their interaction with cellular and mitochondrial thiol groups and Fe2+ metabolism disturbance. Similarities and differences in the toxic effects of Tl+ from those of other heavy metals under review are discussed. Similarities may be due to the increase in the cytoplasmic calcium concentration induced by Tl+ and these metals. One difference discussed is the failure to decrease Tl+ toxicity through metallothionein-dependent mechanisms. Another difference could be the decrease in reduced glutathione in the matrix due to the reversible oxidation of Tl+ to Tl3+ near the centers of ROS generation in the respiratory chain. The latter may explain why thallium toxicity to humans turned out to be higher than the toxicity of mercury, lead, cadmium, copper, and zinc.

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“…Postoji sugestija da je mitohondrijalna disfunkcija najraniji događaj u citotoksičnosti teškim metalima 36 . Od strane drugih autora je istaknuto da se produkcija reaktivnih kiseoničnih radikala (RKR) pokazala kao jedan od prvih koraka u kadmijumom indukovanoj citotoksičnosti koja prethodi mitohondrijalnom oštećenju 35,37 .…”

Section: Diskusijaunclassified

Endocrine pancreas in rats chronically treated with Cadmium

Jancic¹,

Rančić²,

Zujovic³

et al. 2018

Materia medica

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Kadmijum (Cd) je mekan srebtrnasto-beli metal, jedan od 126 prioritetnih zagađivača, a svrstan je i u grupu humanih karcinogena I kategorije.Cilj rada je mikromorfološko i funkcionalno ispitivanje endokrinog pankreasa pacova hronično tretiranih kadmijumom. Za istraživanje su korišćeni beli Wistar pacovi ženskog pola, starosti 35-37 dana, težine 120-140 g.Ukupno je bilo 22 životinje koje su podeljene na kontrolnu (n=11) i eksperimentalnu grupu (n=11). Eksperimentalna grupa je svakodnevno tretirana sa 15mg/kg CdCl2 rastvorenog u pijaćoj vodi. Kontrolna grupa nije bila podvrgnuta nikakvom tretmanu. Svi pacovi su čuvani u kontrolisanim laboratorijskim uslovima. Posle tri meseca, sve životinje su žrtvovane. Tkivo pankreasa je rutinski obrađeno i kalupljeno u parafi n. Na 4μm presecima su primenjene HE i imunohistohemijska ABC metoda sa antitelima na: chromogranin A, insulin,glucagon,somatostatin, pankreasni polipeptid, i peptid YY. U životinja eksperimentalne grupe su nađene guste, hiperplastične B ćelije koje zaposedaju skoro čitavu površinu insule. Prisutna je i hiperplazija A ćelija sa izraženom funkcionalnom aktivnošću. Osim po obodu hiperplastičnih insula, pojedinačne A ćelije se nalaze i u acinusima u kojima je njihova aktivnost znatno povećana. Zapažen je povećan mitotski indeks i odsustvo citoplazmatskih produžetka D ćelija. Izražena je hiperplazija PP ćelija, sa znacima kako morfološkog tako i funkcionalnog polimorfi zma. Prisustvo PP ćelija je evidentirano i u hiperplastičnom i displastičnom epitelu većih duktusa. Samo u životinja eksperimentalne grupe smo našli ćelije koje sekretuju peptid YY. Ove ćelije imaju identičnu topografi ju kao i A ćelije, ali je njihov broj znatno manji. Hronično izlaganje kadmijumu remeti strukturu i funkciju endokrinog pankreasa.Sve pankreasne endokrine ćelije su pogođene.

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Inhibition of cadmium-induced apoptosis by glutathione S-transferase P1 via mitogen-activated protein kinases and mitochondrial pathways

Cited by 11 publications

References 49 publications

Proteomic analysis of bovine mammary epithelial cells after in vitro incubation with S. agalactiae: potential biomarkers

Proteomic analysis of bovine mammary epithelial cells after in vitro incubation with S. agalactiae: potential biomarkers

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Endocrine pancreas in rats chronically treated with Cadmium

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