Decreased Glutathione Peroxidase Activities with Concomitant Increased Oxidized Glutathione Levels among Residents in an Arsenic Contaminated Community of Southern Thailand

Warangkana CHUNGLOK


Glutathione peroxidase (GPx) and glutathione are important antioxidants responsible for the scavenging of reactive oxygen species (ROS). It has been shown that changes in GPx activities and glutathione levels are associated with various diseases including toxic chemical related diseases and cancers. The study aimed to determine the levels of GPx activity and glutathione among residents in Ron Phibun district, an arsenic-exposed area. Blood samples were obtained from 32 volunteers in the Thasala group, a nearby nonarsenic-exposed area and 36 residents in the Ron Phibun group. Red cell lysates were subjected to analysis of GPx activity and glutathione. The results showed that GPx activities were significantly decreased among study subjects from Ron Phibun (p < 0.05). Interestingly, oxidized glutathione (GSSG) levels were significantly increased compared with those from Thasala (p < 0.05). Total glutathione and reduced glutathione (GSH) levels were not different among the two groups. Mean values of GPx activities, total glutathione and GSH tended to decrease among high-exposure subjects compared to low-exposure subjects. This was concomitant with a slight increase in GSSG levels among high-exposure subjects. The levels of GPx activities and GSSG may be early biomarkers for low levels of oxidative stress in a mining area affected with arsenic poisoning.


Glutathione peroxidase, glutathione, antioxidants

Full Text:



CJ Chen, LI Hsu, CH Wang, WL Shih, YH Hsu, MP Tseng, YC Lin, WL Chou, CY Chen, CY Lee, LH Wang, YC Cheng, CL Chen, SY Chen, YH Wang, YM Hsueh, HY Chiou and MM Wu. Biomarkers of exposure, effect, and susceptibility of arsenic-induced health hazards in Taiwan. Toxicol. Appl. Pharmacol. 2005; 206, 198-206.

ZY Shen, WY Shen, MH Chen, J Shen and Y Zeng. Reactive oxygen species and antioxidants in apoptosis of esophageal cancer cells induced by As2O3. Int. J. Mol. Med. 2003; 11, 479-84.

TC Wang, KY Jan, AS Wang and JR Gurr. Trivalent arsenicals induce lipid peroxidation, protein carbonylation, and oxidative DNA damage in human urothelial cells. Mutat. Res. 2007; 615, 75-86.

V Kokilavani, MA Devi, K Sivarajan and C Panneerselvam. Combined efficacies of DL-alpha-lipoic acid and meso 2,3 dimercaptosuccinic acid against arsenic induced toxicity in antioxidant systems of rats. Toxicol. Lett. 2005; 160, 1-7.

S Bashir, Y Sharma, M Irshad, SD Gupta and TD Dogra. Arsenic-induced cell death in liver and brain of experimental rats. Basic Clin. Pharmacol. Toxicol. 2006; 98, 38-43.

S Maiti and AK Chatterjee. Differential response of cellular antioxidant mechanism of liver and kidney to arsenic exposure and its relation to dietary protein deficiency. Environ. Toxicol. Pharmacol. 2000; 8, 227-35.

S Bhadauria and SJ Flora. Response of arsenic-induced oxidative stress, DNA damage, and metal imbalance to combined administration of DMSA and monoisoamyl-DMSA during chronic arsenic poisoning in rats. Cell Biol. Toxicol. 2007; 23, 91-104.

J Pi, H Yamauchi, Y Kumagai, G Sun, T Yoshida, H Aikawa, C Hopenhayn-Rich and N Cjimojo. Evidence for induction of oxidative stress caused by chronic exposure of Chinese residents to arsenic contained in drinking water. Environ. Health Persp. 2002; 4, 331-6.

MM Wu, HY Chiou, TW Wang, YM Hsueh, IH Wank, CJ Chen and TC Lee. Association of blood arsenic levels with increased reactive oxidants and decrease antioxidant capacity in a human population of northeastern Taiwan. Environ. Health Persp. 2001; 10, 1011-7.

B Vitayavirasak, K Rakwong and W Chatchawej. Environmental arsenic exposure of schoolchildren in a former tin mining and smelting community of southern Thailand. Environ. Sci. 2005; 2, 195-205.

S Kapaj, H Peterson, K Liber and P Bhattacharya. Human health effects from chronic arsenic poisoning-a review. J. Environ. Sci. Heal. A Tox. Hazard. Subst. Environ. Eng. 2006; 41, 2399-428.

HM Foy, S Tarmapai, P Eamchan and O Metdilogkul. Chronic arsenic poisoning from well water in a mining area in Thailand. Asia Pac. J. Publ. Health 1992-1993; 6, 150-2.

L Flohe and WA Gunzler. Assays of glutathione peroxidase. Method. Enzymol. 1984; 105, 114-21.

OW Griffith. Determination of glutathione and glutathione disulfide using glutathione reductase and 2-vinylpyridine. Anal. Biochem. 1980; 106, 207-12.

M Valko, CJ Rhodes, J Moncol, M Izakovic and M Mazur. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem. Biol. Interact. 2006; 160, 1-40.

S Shila, V Kokilavani, M Subathra and C Panneerselvam. Brain regional responses in antioxidant system to alpha-lipoic acid in arsenic intoxicated rat. Toxicology 2005; 210, 25-36.

TS Wang, YF Shu, YC Liu, KY Jan and H Huang. Glutathione peroxidase and catalase modulate the genotoxicity of arsenite. Toxicology 1997; 21, 229-37.

S Charoensi, A Ruangtong, A Sanpechuda and W Chunglok. Decreased glutathione peroxidase activities among residents in Ron Phibun. Science and Technology for Global Sustainability. In: Proceedings of the 33rd Congress on Science and Technology of Thailand, Nakhon Si Thammarat, Thailand. 2007.

D Mishra, A Mehta and SJ Flora. Reversal of arsenic-induced hepatic apoptosis with combined administration of DMSA and its analogues in guinea pigs: role of glutathione and linked enzymes. Chem. Res. Toxicol. 2008; 21, 400-7.


  • There are currently no refbacks.

Online ISSN: 2228-835X

Last updated: 20 June 2019