Pesticide exposure on southwestern Taiwanese with MnSOD and NQO1 polymorphisms is associated with increased risk of Parkinson's disease

Fong, Chin-Shih; Wu, Ruey‐Meei; Shieh, Jia‐Ching; Chao, Ya-Ting; Fu, Yi-Ping; Kuao, Chiz-Liang; Cheng, Chun-Wen

doi:10.1016/j.cca.2006.11.006

Cited by 81 publications

(40 citation statements)

References 34 publications

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“…The frequency distributions of C and T alleles were found to be respec- has the similar CC genotype frequency as seen in AfricanAmerican [35], Finn [36], and Italian populations [37]. We detected considerably lower CC genotype frequency than those found in Korean [38], Japan [39], Chinese [40] and Taiwan [41] populations and higher frequencies than those found in American [23], Polish [42], Danish [43], German [44] and Russian [45] populations. Eventually, CC genotype frequency in populations of the eastern countries, were lower (between 0-17%) found than the western countries (between 42-67%) ( Table 4).…”

Section: Resultssupporting

confidence: 75%

Manganese-Superoxide Dismutase (MnSOD) Polymorphisms

Siliğ

Taş²,

Pınarbaşı³

2015

Turk J Bioch

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Objective: Manganese superoxide dismutase (MnSOD,SOD2), the only known superoxide scavenger in mitochondria, may be particularly important for antioxidant defense because mitochondria are the major sites for cellular metabolism and hence production of reactive oxygen species. Methods: In this study, 440 Turkish individuals were genotyped for polymorphisms of SOD2 gene. The distribution of these polymorphisms in this population was examined using a PCR-RFLP method. Results: In the present study, a total of 440(females: 201, 46% and males: 239, 54%) healthy individuals were studied. The mean age of the study population was 54,41±5,76 years (males, 55,34±5,76; females, 53,12±7,16 and males: 239, 54%) unrelated healthy volunteers from central Anatolia. There was no age and sex restriction for selection of the healthy volunteers, who were free of any chronic diseases, living in the same geographic area, and having no history of any cancer. We attempted to include all the control studies published to data on the SOD2 rs4880 polymorphism. DNA isolationTwo milliliters peripheral blood samples were collected in to citrate containing tubes from all subjects. DNA was extracted from whole blood by salting out procedure as soon as the samples reached to laboratory [19]. GenotypingThe distribution of these polymorphisms was examined using a PCR-RFLP method. For amplifying the SOD2 rs4880 polymorphism, forward primer 5'-ACC AGC AGG CAG CTG GCG CCG G-3' and reverse primer 5'-GCG TTG ATG TGA GGT TCC AC-3'were used. PCR reactions contained 0,75 µL (25 pmol/µL) of each primer, 2µL dNTPs (1mmol/L), 1,5µL of 25 mmol/L MgCI2, 1.5 Units of Taq DNA polymerase and 16,2µL sterile deionized water. DNA 50-100 ng is in a total volume of 50 µL. The Statistical analysisAll statistical analyses were performed using the Statistical Package for Social Sciences Program (SPSS, version 11). The Chi-square (X 2 ) test was used to evaluate the association between healthy individuals and SOD genotypes. Genotype, allele frequencies was estimated by counting. Hardy-Weinberg equilibrium between expected and observed genotype distributions was assessed using the X

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Section: Resultssupporting

confidence: 75%

Manganese-Superoxide Dismutase (MnSOD) Polymorphisms

Siliğ

Taş²,

Pınarbaşı³

2015

Turk J Bioch

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“…The unique role of NQO1 in detoxification of electrophilic quinone molecules and ROS suggests that this phase 2 enzyme may play an important part in protecting against dopaminergic neurodegeneration in PD patients. In this context, polymorphism of NQO1 has been suggested to be associated with an increased risk of developing PD (Fong et al, 2007). In addition to NQO1, GSH is also capable of reacting with quinone molecules as well as ROS to attenuate dopamine or 6-OHDA-induced cytotoxicity (Shimizu et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Potent induction of total cellular GSH and NQO1 as well as mitochondrial GSH by 3H-1,2-dithiole-3-thione in SH-SY5Y neuroblastoma cells and primary human neurons: Protection against neurocytotoxicity elicited by dopamine, 6-hydroxydopamine, 4-hydroxy-2-nonenal, or hydrogen peroxide

et al. 2008

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Evidence suggests oxidative and electrophilic stress as a major factor contributing to the neuronal cell death in neurodegenerative disorders, especially Parkinson's disease. Consistent with this concept, administration of exogenous antioxidants has been shown to be protective against oxidative/ electrophilic neurodegeneration. However, whether induction of endogenous antioxidants and phase 2 enzymes by the unique chemoprotectant, 3H-1,2-dithiole-3-thione (D3T) in neuronal cells also affords protection against oxidative and electrophilic neurocytotoxicity has not been carefully investigated. In this study, we showed that incubation of SH-SY5Y neuroblastoma cells or primary human neurons with micromolar concentrations (10-100 μM) of D3T for 24 h resulted in significant increases in the levels of reduced glutathione (GSH) and NAD(P)H:quinone oxidoreductase 1 (NQO1), two crucial cellular defenses against oxidative and electrophilic stress. D3T treatment also caused increases in mRNA expression of γ-glutamylcysteine ligase catalytic subunit and NQO1 in SH-SY5Y cells. In addition, D3T treatment of the neuronal cells also resulted in a marked elevation of GSH content in the mitochondrial compartment. To determine the protective effects of the D3T-induced cellular defenses on neurotoxicant-elicited cell injury, SH-SY5Y cells were pretreated with D3T for 24 h and then exposed to dopamine, 6-hydroxydopamine (6-OHDA), 4-hydroxy-2-nonenal (HNE), or H 2 O 2 , agents that are known to be involved in neuron degeneration. We observed that D3T-pretreatment of SH-SY5Y cells led to significant protection against the cytotoxicity elicited by the above neurotoxicants. Similar neurocytoprotective effects of D3T-pretreatment were also observed in primary human neurons exposed to 6-OHDA or HNE. Taken together, this study demonstrates that D3T potently induces neuronal cellular GSH and NQO1 as well as mitochondrial GSH, and that such upregulated endogenous defenses are accompanied by increased resistance to oxidative and electrophilic neurocytotoxicity.

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“…Whereas Stoehlmacher et al (21) (25), schizophrenia (26), etc.] Homozygosity for Ala has been found to be a major risk factor for severe alcoholic liver disease (27).…”

mentioning

confidence: 99%