Biological evaluation of new nickel(II) metallates: Synthesis, DNA/protein binding and mitochondrial mediated apoptosis in human lung cancer cells (A549) via ROS hypergeneration and depletion of cellular antioxidant pool

Kalaivani, P.; Saranya, Sithuraj; Poornima, Paramasivan; Prabhakaran, R.; Dallemer, F.; Padma, Viswanadha Vijaya; Natarajan, K.

doi:10.1016/j.ejmech.2014.05.075

Cited by 92 publications

(55 citation statements)

References 97 publications

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“…Case-control studies found GSTP1 exon 5 polymorphisms to be associated with lung cancer risk (2). However, other research results suggested that GSTP1 polymorphisms were not statistically associated with lung cancer risk (15,17).…”

Section: Discussionmentioning

confidence: 81%

“…Related studies have also confirmed this finding. It has been demonstrated that GSTP1 exon 5 Val allele decreases the GSTP activity, and that higher levels of hydrophobic DNA adducts are present in the lung tissue in individuals with low activity alleles (17), in addition to increased levels of PAH-DNA adducts in peripheral blood lymphocytes (18). The GSTP1 exon 5 polymorphisms change the structure, function and expression level of GSTP1, alter the body's ability to detoxify carcinogens, and affect individual susceptibility to lung cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, GSTP1 plays an important role in the detoxification of inhaled carcinogens, such as activated polycyclic aromatic hydrocarbons (PAHs), benzo(a)pyrene and tobacco carcinogens (16). It has even been suggested to be the most important GST influencing lung cancer risk (17). The GSTP1 gene has polymorphisms in exon 5.…”

Section: Discussionmentioning

confidence: 99%

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Correlation between metabolic enzyme GSTP1 polymorphisms and susceptibility to lung cancer

Wang

Ren

Zhang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to determine the frequency distribution and characteristics of polymorphic alleles and genotypes in glutathione S-transferase π 1 (GSTP1) exon 5, and to explore the correlation between GSTP1 exon 5 polymorphisms and susceptibility to lung cancer using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Patients were diagnosed with lung cancer from May 2006 to October 2008 by postoperative pathological examination. A total of 150 patients, including 115 males and 35 females, aged 31-76 years (mean, 57.1 years) were enrolled. The control group consisted of 152 healthy volunteers who received physical examination at outpatient clinics. Genomic DNA was extracted from the peripheral venous blood of the 302 subjects, and the GSTP1 genotype was determined by PCR-RFLP and restricted enzyme digestion of PCR products. GSTP1 polymorphisms were analyzed in the 302 subjects. The C and G allele frequencies of GSTP1 in the control and lung cancer groups showed no significant difference (P=0.135); the frequencies of three different genotypes, A/A, A/G and G/G, of GSTP1 in the control and lung cancer groups exhibited no significant differences between the two groups (P=0.223). GSTP1 genotype frequencies in the study population fitted the Hardy-Weinberg equilibrium, demonstrating that the genotype results of this study conform to this genetic law. Overall, 50.7% of the subjects in the lung cancer group carried the non-A/A genotype of GSTP1, which was higher than the 43.4% of the control group. The risk of lung cancer in subjects with the non-A/A genotype was 1.43-fold higher than that in those with the A/A genotype, but no statistical significance was found (P=0.138). GSTP1 exon 5 polymorphisms were demonstrated to be associated with lung cancer susceptibility on the whole. However, stratified analysis suggested the correlation of GSTP1 exon 5 polymorphisms with lung squamous cell carcinoma risk, and that exon 5 polymorphisms might increase the risk of lung squamous cell carcinoma. Exon 5 GSTP1 polymorphisms were not found to be a strong influencing factor in lung cancer risk, but may play a certain role.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

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Correlation between metabolic enzyme GSTP1 polymorphisms and susceptibility to lung cancer

Wang

Ren

Zhang

et al. 2015

Experimental and Therapeutic Medicine

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“…It has been convinced that GSH and LDH play a key role in the intrinsic pathway-mediated apoptosis (Kalaivani, et al 2014). Under normal physiological conditions, antioxidant systems balance reactive oxygen species (ROS) and LDH production and prevent oxidative damage encountered by cells.…”

Section: Discussionmentioning

confidence: 99%

Wogonin Prevents Rat Dorsal Root Ganglion Neurons Death via Inhibiting Tunicamycin-Induced ER Stress In Vitro

Zhao

et al. 2014

Cell Mol Neurobiol

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Wogonin is a natural flavonoid isolated from the root of Scutellaria baicalensis Georgi, which has been widely used in various research areas for its anti-oxidant, anti-inflammatory, and anti-cancer activities. It also presents a neuroprotective effect in the brain while encounters stress conditions, but the mechanisms controlling the neuroprotective effect of wogonin are not clear. In this study, we investigated the biomechanism underlying the neuroprotective effect of wogonin on rat dorsal root ganglion (DRG) neurons. Wogonin pre-treatment at 75 μM significantly increased the cell viability of DRG neurons and decreased the number of the propidium iodide-positive DRG neurons before the endoplasmic reticulum (ER) stress is being induced by tunicamycin (TUN) (0.75 μg/mL). In addition, Wogonin also inhibited the release of LDH and up-regulated the level of GSH. Furthermore, wogonin decreased the activation of ER stress-related molecules, including glucose-regulated protein 78 (GRP78), GRP94, C/EBP-homologous protein, active caspase12 and active caspase3, phosphorylation of pancreatic ER stress kinase, and eukaryotic initiation factor 2 alpha (eIF2α). In summary, our results indicated that wogonin could protect DRG neurons against TUN-induced ER stress.

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“…Some biological features of these thiosemicarbazone complexes such as the palladium(II) complexes (antimalarial and anticancer agents) [13,14], ruthenium(II) complexes (antimicrobial) [15], and a nickel(II) complex with DNA binding ability [16] were investigated. In a study [17], the influences of nickel(II)-PPh 3 complexes with some methoxy-substituted thiosemicarbazones on mitochondrial mediated apoptosis in human lung cancer cells (A549) via ROS hyper-generation were tested.…”

Section: Introductionmentioning

confidence: 99%

Spectroscopic, electrochemical and X-ray diffraction studies on nickel(II)-complexes of acetophenone thiosemicarbazones substituted six-carbon groups

Güveli

Özdemir

Koca

et al. 2016

Inorganica Chimica Acta

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Biological evaluation of new nickel(II) metallates: Synthesis, DNA/protein binding and mitochondrial mediated apoptosis in human lung cancer cells (A549) via ROS hypergeneration and depletion of cellular antioxidant pool

Cited by 92 publications

References 97 publications

Correlation between metabolic enzyme GSTP1 polymorphisms and susceptibility to lung cancer

Correlation between metabolic enzyme GSTP1 polymorphisms and susceptibility to lung cancer

Wogonin Prevents Rat Dorsal Root Ganglion Neurons Death via Inhibiting Tunicamycin-Induced ER Stress In Vitro

Spectroscopic, electrochemical and X-ray diffraction studies on nickel(II)-complexes of acetophenone thiosemicarbazones substituted six-carbon groups

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