• Korean Journal of Environmental Biology
• /
• v.41 no.4
• /
• pp.386-399
• /
• 2023

Microplastics and nanoplastics (NMPs) are considered one of hazardous contaminants in marine ecosystems due to their toxic effects, such as reproduction disorder and oxidative stress, on marine organisms. Although water temperature is rising due to global climate change, little information on the toxicological interaction between NMPs and temperature is available. Therefore, in this study, we confirmed the toxicity of NMPs (polystyrene [PS] beads; 0.05- and 6-㎛) on brackish water fleas (Diaphanosoma celebensis) depending on increased temperature (30℃ and 35℃) at individual and molecular levels. In the chronic toxicity test, the group exposed to high temperatures showed an earlier first reproduction time compared to the normal temperatures group, but it was delayed by co-exposure to NMPs at 35℃. Notably, the total reproduction decreased significantly only after 0.05-㎛ PS beads exposure at 30℃. Interaction analysis showed that first reproduction time, modulation of the antioxidant-related gene (GSTS1), heat shock gene (Hsp70), and ecdysteroid pathway-related genes (EcR_A, EcR_B, and CYP314A1) were closely related to temperature and PS beads size. These results indicate that microplastics have size-dependent toxicity, and their toxicity can be enhanced at high temperatures. In addition, higher temperatures and PS beads exposure may have negative effects on reproduction. This study suggests that various factors such as water temperature should be considered when evaluating the toxicity of microplastics in marine ecosystems, and provides an understanding of the complex toxic interaction between water temperature and microplastics for marine zooplankton.

• Asian Pacific Journal of Cancer Prevention
• /
• v.13 no.1
• /
• pp.325-328
• /
• 2012

Objective: Glutathione S-transferases (GSTs) are important enzymes that are involved in detoxification of environmental carcinogens. Molecular epidemiological studies have been conducted to investigate the association between GSTM1 and GSTT1 homozygous deletion polymorphisms and brain tumours but results have been conflicting. The aim of this study was to clarify this problem using a meta-analysis. Methods: A total of 9 records were identified by searching the PubMed and Embase databases. Fixed- and random-effects models were performed to estimate the pooled odds ratios. Results: No significant association was found between the GSTM1 and GSTT1 homozygous deletion polymorphisms and risk of brain tumours, including glioma and meningioma. Similar negative results were also observed in both population-based and hospital-based studies. Conclusion: These findings indicate that the GSTM1 and GSTT1 polymorphisms may not be related to the development of brain tumours.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.6
• /
• pp.3861-3864
• /
• 2013

Glutathione S-transferase (GST) enzyme levels are associated with risk of many cancers, including hematologic tumours. We here aimed to investigate the relationships between GSTM1, GSTT1 and GSTP1 polymorphisms and the risk of AML. Genotyping of GSTs was based upon duplex polymerase-chain-reactions with the confronting-two-pair primer (PCR-CTPP) method in 163 cases and 204 controls. Individuals carrying null GSTT1 genotype had a 1.64 fold risk of acute leukemia relative to a non-null genotype (P<0.05). A heavy risk was observed in those carrying combination of null genotypes of GSTM1 and GSTT1 and GSTP1 Val allele genotypes when compared with those carrying wild genotypes, with an OR (95% CI) of 3.39 (1.26-9.26) (P<0.05). These findings indicate that genetic variants of GST and especially the GSTT1 gene have a critical function in the development of AML. Our study offers important insights into the molecular etiology of AML.

• International Journal of Industrial Entomology and Biomaterials
• /
• v.18 no.1
• /
• pp.28-32
• /
• 2009

We describe here the cloning and characterization of a cDNA encoding the glutathione S-transferase (GST) from the bumblebee Bombus ignitus. The Delta-class B. ignitus GST (BiGSTD) gene spans 1668 bp and consists of four introns and five exons that encode 216 amino acid residues with a calculated molecular weight of approximately 24561 Da and a pI of 8.03. The N-terminal domain of BiGSTD has a conserved Ser residue, as well as conserved Lys, Pro, Glu, Ser and Tyr residues that are involved in the GSH-binding site of GST. The BiGSTD showed 60% protein sequence identity to the Bombyx mori GSTT1, 58% to Musca domestica GST, 57% to Drosophila melanogaster GST, and 55% to Anopheles gambiae GST1. BiGSTD was close to the insect-specific Delta class of GSTs in a phylogenetic tree. Northern blot analysis showed that BiGSTD is highly expressed in the fat body and midgut, and less so in the muscles of B. ignitus worker bees.

• Proceedings of the Korean Society of Food Science and Nutrition Conference
• /
• 2004.11a
• /
• pp.53-60
• /
• 2004

The pro-apoptotic effect of phenethyl isothiocyanate (PEITC) and the role of glutathione (GSH) in sulforaphane (SFN)-induced antioxidant response element-dependent gene expression were investigated. The caspase-3 and caspase-9 activities were stimulated by PEITC. The release of cytochrome c was time- and dose- dependent. SP600125 suppressed apoptosis induced by PEITC. Similarly, this JNK inhibitor attenuated both cytochrome c release and caspase-3 activation induced by PEITC. SFN is converted to the glutathione conjugate by glutathione S-transferases (GSTs). It was accumulated in mammalian cells by up to several hundred-fold over the extracellular concentration, by conjugation with intracellular GSH. The induction of ARE by SFN was 8.6-fold higher than by SFN-NAC. The decrease in ARE expression at higher concentrations of SFN and SFN-NAC was correlated with the accelerated apoptotic cell death, with a dose-dependent activation of caspase 3 activity by SFN. Upon addition of extracellular GSH within 6 hr of treatment with SFN, the effect on ARE expression was blocked almost completely.

• Journal of Environmental Health Sciences
• /
• v.36 no.1
• /
• pp.1-13
• /
• 2010

Evidences supporting gene-environment interaction are accumulating in terms of environmental exposure including lifestyle factors and related genetic variants. One form of defense mechanism against cancer development involves a series of genes whose role is to metabolize (activation/detoxification) and excrete potentially toxic compounds and to repair subtle mistakes in DNA. The purpose of this article is to provide a brief review of the notion of gene-environment interaction, environmental/occupational carcinogens and related cancers, and previous studies of gene-environment interaction on cancers caused by exposure to carcinogenesis. With a number of studies on the interaction between lifestyle factors (e.g., smoking and diet) and genetic polymorphisms in genes involved in xenobiotic metabolism and DNA repair excluded, only several studies have been conducted on the interactive effects between polymorphisms of CYPs, GSTs, ERCCs, XRCCs and environmental/occupational carcinogens such as vinyl chloride, benzo[a]pyrene, and chloroform on carcinogenesis or genotoxicity. Future studies may need to be conducted with sufficient number of subjects and based on occupational cohorts to provide useful information in terms of advanced risk assessment and regulation of exposure level.

• Molecular & Cellular Toxicology
• /
• v.3 no.1
• /
• pp.11-18
• /
• 2007

Mechanisms of insecticide resistance found in insects may include three general categories. Modified behavioral mechanisms can let the insects avoid the exposure to toxic compounds. The second category is physiological mechanisms such as altered penetration, rapid excretion, lower rate transportation, or increased storage of insecticides by insects. The third category relies on biochemical mechanisms including the insensitivity of target sites to insecticides and enhanced detoxification rate by several detoxifying mechanisms. Insecticides metabolism usually results in the formation of more water-soluble and therefore more readily eliminated, and generally less toxic products to the host insects rather than the parent compounds. The representative detoxifying enzymes are general esterases and monooxygenases that catalyze the toxic compounds to be more water-soluble forms and then secondary metabolism is followed by conjugation reactions including those catalyzed by glutathione S-transferases (GSTs). However, a change in the resistant species is not easily determined and the levels of mRNAs do not necessarily predict the levels of the corresponding proteins in a cell. As genomics understands the expression of most of the genes in an organism after being stressed by toxic compounds, proteomics can determine the global protein changes in a cell. In this present review, it is suggested that the environmental proteomic application may be a good approach to understand the biochemical mechanisms of insecticide resistance in insects and to predict metabolomic changes leading to physiological changes of the resistant species.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2001.10a
• /
• pp.191-192
• /
• 2001

Although the incidence rates of gastric cancer and liver cancer, the most common cancers in Korea, are tending decrease, lung cancer is on the increase every year as cause of cancer death as well as incidence rate in Korea. And cigarette smoke is believed to be responsible for 90% of lung cancer. Many investigators have reported an association between genetic polymorphism of cytochromes P-450 (CYPs) or glutathoine S-transferase (GSTs) and susceptibility to lung cancer.(omitted)

• Journal of Embryo Transfer
• /
• v.25 no.4
• /
• pp.273-279
• /
• 2010

Follicular cystic follicles (FCFs) show delayed regression with persistent follicle growth. However, the mechanism by which follicles are persistently grown remains unclear. Glutathione S-transferases (GSTs) are drug-metabolizing and detoxification enzymes that are involved in the intracellular transport and metabolism of steroid hormones. In this study, a proteomic analysis was performed to identify whether GST expression is changed in bovine FCFs and to predict the interactions between GST and other proteins. Normal follicles and FCFs were classified based on their sizes (5 to 10 mm and 25 mm). In bovine follicles, GST mu 1 (GSTM1) was detected as a differentially expressed protein (DEP) and significantly up-regulated in FCFs compared to normal follicles (p<0.05). Consistent with the proteomic results, semi-quantitative PCR data and western blot analysis revealed an up-regulation of GSTM1 in FCFs. Expression levels of aromatase and dehydrogenase proteins were changed in FCFs. These results show that the up-regulation of GSTM1 that is observed in bovine FCFs is likely to be responsible for the persistent follicle growth in FCFs as the activity of aromatase and the dehydrogenases.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.4
• /
• pp.2221-2224
• /
• 2013

The glutathione S-transferases (GSTs) are a family of enzymes involved in the detoxification of a wide range of chemicals, including important environmental carcinogens, as well as chemotherapeutic agents. In the present study 294 acute leukemia cases, comprising 152 of acute lymphocytic leukemia (ALL) and 142 of acute myeloid leukemia, and 251 control samples were analyzed for GSTM1 and GSTT1 polymorphisms through multiplex PCR methods. Significantly increased frequencies of GSTM1 null genotype (M0), GSTT1 null genotype (T0) and GST double null genotype (T0M0) were observed in the both ALL and AML cases as compared to controls. When data were analyzed with respect to clinical variables, increased mean levels of WBC, Blast %, LDH and significant reduction in DFS were observed in both ALL and AML cases with T0 genotype. In conclusion, absence of both GST M & GST T might confer increased risk of developing ALL or AML. The absence of GST enzyme might lead to oxidative stress and subsequent DNA damage resulting in genomic instability, a hallmark of acute leukemia. The GST enzyme deficiency might also exert impact on clinical prognosis leading to poorer DFS. Hence GST genotyping can be made mandatory in management of acute leukemia so that more aggressive therapy such as allogenic stem cell transplantation may be planned in the case of patients with a null genotype.