{"refrec":{"BRefID":33280,"RR":"<b>Pane, E.F.; Richards, J.G.; Wood, C.M.</b> (2003). Acute waterborne nickel toxicity in the rainbow trout (<i>Oncorhynchus mykiss</i>) occurs by a respiratory rather than ionoregulatory mechanism. <i>Aquat. Toxicol. 63(1)</i>: 65-82. <a href=\"https://dx.doi.org/10.1016/S0166-445X(02)00131-5\" target=\"_blank\">https://dx.doi.org/10.1016/S0166-445X(02)00131-5</a>","BEntID":33280,"PublicFlag":1,"CheckedFlag":0,"wosflag":1,"vabbflag":0,"RefStringPartII":". <i>Aquat. Toxicol. 63(1)</i>: 65-82. <a href=\"https://dx.doi.org/10.1016/S0166-445X(02)00131-5\" target=\"_blank\">https://dx.doi.org/10.1016/S0166-445X(02)00131-5</a>","DocTypID":8,"DocType":"Journal article","MarineFlag":0,"FreshFlag":0,"BrackishFlag":0,"TerrestrialFlag":0,"Authorstring":"Pane, E.F.; Richards, J.G.; Wood, C.M.","OrigTitleTranslFlag":0,"Authorstringtrunc":"Pane, E.F.; Richards, J.G.; Wood, C.M.","Englishabstract":"The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (<i>Oncorhynch mykiss</i>) Lake Ontario water, where the 96-h LC<sub>50</sub> for juvenile trout (1.5-3.5 g) was 15.3 mg (12.7-19.0, 95% C.L.) dissolved Ni <sup>l-1</sup>. No marked impact of Ni exposure on average unidirectional or net fluxes of Na<sup>+</sup>, Cl<sup>-</sup>, or Ca<sup>2+</sup> was observed in juvenile trout exposed for 48-60 h to 15.6 mg Ni l<sup>-1</sup> as NiSO<sub>4</sub>. Furthermore, when adult rainbow trout (200-340 g) were fitted with indwelling dorsal aortic catheters and exposed for 117 h to 11.6 mg Ni l<sup>-1</sup> as NiSO<sub>4</sub>, plasma ions (Na<sup>+</sup>, Cl<sup>-</sup>, Ca<sup>2+</sup>, and Mg<sup>2+</sup>) were all well conserved. However, mean arterial oxygen tension dropped gradually to ~35% of control values. This drop in P<sub>aO2</sub> was accompanied by an acidosis primarily of respiratory origin. P<sub>aCO2</sub> rose to more than double control values with a concomitant drop in arterial pH of 0.15 units. Acute respiratory toxicity was further evidenced by a significant increase in hematocrit (Ht), and plasma lactate, and a significant decrease in spleen hemoglobin (Hb). Following 117 h of exposure to 11.6 mg Ni l<sup>-1</sup>, the gill, intestine, plasma, kidney, stomach, and heart accumulated Ni significantly, with increases of 60, 34, 28, 11, 8, and 3-fold, respectively. Brain, white muscle, liver, and bile did not significantly accumulate Ni. Plasma Ni exhibited a remarkable linear increase with time to levels approximately 30-fold higher than controls. We conclude that in contrast to most other metals, Ni is primarily a respiratory, rather than an ionoregulatory, toxicant at exposure levels close to the 96-h LC<sub>50</sub>. The implications of a waterborne metal as an acute respiratory toxicant (as opposed to ionoregulatory toxicants such as Cu, Ag, Cd, or Zn) with respect to toxicity modeling are discussed.","AbstractOtherLang":null,"BibLvlCode":"AS","StandardTitle":"Acute waterborne nickel toxicity in the rainbow trout (<i>Oncorhynchus mykiss</i>) occurs by a respiratory rather than ionoregulatory mechanism","OrigTitleLangCode":"en","OrigTitleLangCodeExtended":"eng","OrigTitleLangID":15,"DateLastModified":{"date":"2026-06-14 01:31:05.577823","timezone_type":1,"timezone":"+02:00"},"UserAccessRight":null,"UserAccID":null,"AuthorKeywords":null,"OtherDescriptors":"Rainbow trout; Waterborne; Respiratory toxicity; Ionoregulation","Notes":null,"AnaPub":2003,"MonPub":null,"DateUpdate":"2019-08-05","DateCreate":"2003-03-20","SecASFANote":null,"ConfID":null,"PeerRev":1,"VlizCoreFlag":1,"WoScode":"WOS:000181493000005","VABBcode":null,"OpenAcc":0,"DOI":"10.1016/S0166-445X(02)00131-5"},"refs":null,"anarec":{"AnaID":33280,"PubliDate":2003,"Pagination":"65-82","XtraPublOfAnaID":null,"ISBN":null,"Volume":"63","Issue":"1","BRefMon":null,"BRefMonRR":null,"BRefXtra":null,"BRefXtraRR":null,"SerBRefID":42203,"SerRR":"Aquatic Toxicology. 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