05121nas a2200421 a 4500 20260818095214.0 080625s2007 th uu|m rtt 0| a1eng d .b10746043 AIT Diss. no.EV-07-04 Karnjana Hrimpeng The effects of arsenic on oxidative stress responses in Xanthomonas campestris pv. phaseoli Pathum Thani, Thailand : Asian Institute of Technology, 2007 103 p. : ill. Dissertation ; no. EV-07-04 A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Environmental Engineering and Management Inter-University Program on Environmental Toxicology, Technology and Management Thesis (Ph.D.) - Asian Institute of Technology - Chulabhorn Research Institute - Mahidol University, 2007 Being used as an insecticide and herbicide, arsenic is one of the first priority environmental pollutants contaminated in many agricultural soils. The oxidative stress responses of Xanthomonas campestris pv. phaseoli (Xp), a soil borne phytopathogenic bacteria, against the arsenic exposure were investigated. Pretreatment of Xp with sub-lethal concentrations of sodium arsenite [NaAsO2, As(III)] could induced cross protection against subsequent exposure to lethal doses of hydrogen peroxide (H202) and cumene hydroperoxide (CuOOH) but could not induced the protection against subsequence exposure to menadione (a superoxide generator). This implied that challenging the Xp with low concentrations of As(III) could trigger the defense mechanisms against peroxide rather than superoxide toxicity. The components and genes involved in As(III)-induced cross protection against oxidants killing were investigated. The results demonstrated that these protections were likely due to elevated scavenging enzyme levels including monofunctional catalase (KatA), alkyl hydroperoxide reductase (AhpC), and organic hydroperoxide resistance protein (Ohr). In addition, it was found that katA and ahpC genes play a role in As(III)-induced cross protection from H2O2 killing whereas the ohr and ahpC genes involved in As(III)-induced cross protection from CuOOH killing. Moreover, a mechanism responsible for As(III) toxicity in Xp was determined and found that the metalloid toxicity involved the increased production and accumulation of reactive oxygen species (ROS) including H20 2 and organic hydroperoxide. Finally, the effects of ROS scavenging enzymes on metals exposure were investigated. The result from As(III) sensitivity test against wild type Xp and various mutants, including Xp oxyR, Xp katA, Xp ahpC, Xp katA ahpC, Xp ohr, Xp ohr ahpC, and Xp gor, demonstrated that the peroxide detoxification enzymes are likely to play a physiological role on protecting Xp from As(III) toxicity. It is possible that generation of ROS ability of As(III) is one of the mechanisms responsible for As(III) toxicity. The effect of the ROS scavenging enzymes, catalase and AhpC, on mercury exposure were also investigated in wild type Xp and mutants including Xp HR (constitutively expression of catalase and AhpC), Xp oxyR, Xp katA, and Xp katA ahpC. By contrast, it was found that the mutants whose posses lower levels of catalase or AhpC were more resistant to mercury compared to those of wild type. This result indicated that Xp catalase and AhpC are likely to increase sensitivity of Xp to mercury toxicity. It is possible that these enzymes are involved in mercury cycling by converting less toxic form of mercury (Hg0) into more toxic form (Hg2+) as observed in Escherichia coli. The data elucidate that accumulated As(III) in the environment could alter the responses against oxidative stress in soil phytopathogenic bacteria. As a consequence, this alteration may affect plant-microbe interaction leading to change in bacterial pathogenesis. Arsenic Toxicology Arsenic Environmental aspects Skorn Mongkolsuk, Chairperson Preeda Pakpian, Examination Committee Paiboon Vattanaviboon, Examination committee Rojana Sukchawalit, Examination committee Buttner, Mark, Examination committee Chulabhorn Research Institute / Mahidol University / AIT Fellowship (CRI - MU- AIT), Scholarship donor Asian Institute of Technology. Dissertation ; no. EV-07-04 Full-Text http://203.159.5.9/ait-thesis/detail.php?q=B10445 .b10746043 mnait u 240403 1 080625 m a u 4 mnait mnarc 22 40 Barcode : 30050120725840 CREATED : 2012-08-16 RECORD # : i12687637 LPATRON : 0 LCHKIN : - # RENEWALS : 0 # OVERDUE : 0 IUSE3 : 0 TOT CHKOUT : 0 TOT RENEW : 0 Barcode : 30050160004411 CREATED : 2016-02-02 RECORD # : i12877050 LPATRON : 0 LCHKIN : - # RENEWALS : 0 # OVERDUE : 0 IUSE3 : 0 TOT CHKOUT : 0 TOT RENEW : 0 35015 35015 0 0 0 0 MAIN MAIN mnait 2026-08-18 0 AIT Diss. no.EV-07-04 30050120725840 2026-08-18 09:52:14 3 2026-08-18 22 0 0 0 0 MAIN MAIN mnarc 2026-08-18 0 AIT Diss. no.EV-07-04 30050160004411 2026-08-18 09:52:14 2026-08-18 40