title: Toxicological assessment of indium nitrate on aquatic organisms and investigation of the effects on the PLHC-1 fish cell line.
abstract: Indium nitrate is mainly used as a semiconductor in batteries, for plating and other chemical and medical applications. There is a lack of available information about the adverse effects of indium compounds on aquatic organisms. Therefore, the toxic effects on systems from four trophic levels of the aquatic ecosystem were investigated. Firstly, the bacterium Vibrio fischeri, the alga Chlorella vulgaris and the cladoceran Daphnia magna were used in the toxicological evaluation of indium nitrate. The most sensitive model was V. fischeri, with a NOAEL of 0.02 and an EC(50) of 0.04 mM at 15 min. Although indium nitrate should be classified as harmful to aquatic organisms, it is not expected to represent acute risk to the aquatic biota. Secondly, PLHC-1 fish cell line was employed to investigate the effects and mechanisms of toxicity. Although protein content, neutral red uptake, methylthiazol metabolization, lysosomal function and acetylcholinesterase activity were reduced in cells, stimulations were observed for metallothionein levels and succinate dehydrogenase and glucose-6-phosphate dehydrogenase activities. No changes were observed in ethoxyresorufin-O-deethylase activity. To clarify the main events in PLHC-1 cell death induced by indium nitrate, nine modulators were applied. They were related to oxidative stress (alpha-tocopherol succinate, mannitol and sodium benzoate), disruption of calcium homeostasis (BAPTA-AM and EGTA), thiol protection (1,4-dithiotreitol), iron chelation (deferoxiamine) or regulation of glutathione levels (2-oxothiazolidine-4-carboxylic acid and malic acid diethyl ester). The main morphological alterations were hydropic degeneration and loss of cells. At least, in partly, toxicity seems to be mediated by oxidative stress, and particularly by NADPH-dependent lipid peroxidation.
authors.affiliation: National Institute of Toxicology and Forensic Sciences, Av Dr Fedriani s/n, 41009, Seville, Spain.
authors.forename: Jorge L
authors.initials: JL
authors.lastname: Zurita
authors.forename: Angeles
authors.initials: A
authors.lastname: Jos
authors.forename: Ana
authors.initials: A
authors.lastname: del Peso
authors.forename: Manuel
authors.initials: M
authors.lastname: Salguero
authors.forename: Ana M
authors.initials: AM
authors.lastname: Cameán
authors.forename: Miguel
authors.initials: M
authors.lastname: López-Artíguez
authors.forename: Guillermo
authors.initials: G
authors.lastname: Repetto
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D048908:Aliivibrio fischeri / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D045744:Cell Line, Tumor; D002708:Chlorella / Q000187:drug effects* / Q000254:growth & development; D003621:Daphnia / Q000187:drug effects* / Q000502:physiology; D029941:Fish Proteins / Q000378:metabolism; D005399:Fishes; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D007204:Indium / Q000633:toxicity*; D049449:Luminescence; D009499:Neutral Red / Q000378:metabolism; D009566:Nitrates / Q000633:toxicity*; D019055:No-Observed-Adverse-Effect Level; D013385:Succinate Dehydrogenase / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000633:toxicity*