title: Oxidative DNA damage induced by iron chloride in the larvae of the lace coral Pocillopora damicornis.
abstract: Biochemical and molecular biomarkers tools are utilized as early warning signatures of contaminant exposure to target and non-target organisms. The objective of this study was to investigate the sublethal effects of iron chloride to the larvae of the lace coral Pocillopora damicornis by measuring a suit of oxidative-stress biomarkers. The larvae were exposed to a range of sublethal concentrations of iron chloride (0.01, 0.1, 1, 10, and 100 ppm) for seven days. With reference to oxidative stress biomarkers, the no-observed effect concentration (NOEC) and the lowest observed effect concentration (LOEC) of iron chloride were observed to be 0.01 and 100 ppm respectively. At the end of the seventh day the antioxidant status of the larvae was evaluated by the levels of glutathione (GSH), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione-S-transferase (GST), in both experimental and control groups. For the quantification of cellular oxidative damage, lipid peroxidation (LPO) activity was determined in the same and the extent of DNA damage was assessed by the expression of DNA apurinic/apyrimidinic (AP) sites. Iron chloride exhibited a concentration-dependent inhibition of GSH and GPX and induction of GR, GST, LPO, and DNA-AP sites in the P. damicornis larvae when compared to the control group. The oxidative stress biomarkers of the larvae exposed to 0.1, 1, and 10 ppm of iron chloride did not show any significant overall differences when compared to the control group. However the activities of LPO, GSH, GPX, GR, GST and DNA-AP in the larval group exposed to 100 ppm of iron chloride exhibited statistically significant (P=0.002, 0.003, 0.002, 0.002, 0.005 and 0.007) differences when compared to the control group. The research results indicated that iron chloride in concentrations at the 100 ppm level caused oxidative stress in the P. damicornis larvae.
authors.affiliation: Kewalo Marine Laboratory, Pacific Biosciences Research Center, University of Hawaii at Manoa, 41 Ahui Street, Honolulu, HI 96813, USA. vijayavelkannappan@gmail.com
authors.forename: K
authors.initials: K
authors.lastname: Vijayavel
authors.forename: C A
authors.initials: CA
authors.lastname: Downs
authors.forename: G K
authors.initials: GK
authors.lastname: Ostrander
authors.forename: R H
authors.initials: RH
authors.lastname: Richmond
mesh_terms: D000818:Animals; D037421:Anthozoa / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D000975:Antioxidants / Q000378:metabolism; D001080:Apurinic Acid / Q000235:genetics; D002712:Chlorides / Q000633:toxicity*; D004249:DNA Damage; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D058085:Iron Compounds / Q000633:toxicity*; D007814:Larva / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D019055:No-Observed-Adverse-Effect Level; D018384:Oxidative Stress / Q000187:drug effects*; D011119:Polynucleotides / Q000235:genetics; D013997:Time Factors
chemical_list: D000975:Antioxidants; D002712:Chlorides; D058085:Iron Compounds; D011119:Polynucleotides; C001790:apyrimidinic acid; D001080:Apurinic Acid; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione