The decline in glucose is most likely a result of withholding feed during acclimation and experimentation and the exhaustion of energy stores. Brown et al. reported a similar alteration in plasma glucose in catheterized PI-103 rainbow trout and attributed it to withholding feed. There was no effect of waterborne Mo exposure on hematocrit. The results of this study are in XAV939 in vivo concordance with data from a chronic waterborne exposure of up to 17 mg l-1 reporting no change in hematocrit in various life stages of rainbow trout. Findings outlined by McConnell regarding observations of fused gill lamellae in rainbow trout and by Reid regarding increased ventilation and mucus production in kokanee salmon during Mo exposure, however, would preclude one to think that these manifestations would have an effect on hematocrit. According to Heath, any pollutant that results in gill damage and subsequent internal hypoxia can be expected to increase hematocrit. This indicates that waterborne Mo, despite irritating the gills, does not induce internal hypoxia. This is also true of the metal lead. When Hodson et al. and Martinez et al. exposed rainbow trout and Prochilodus lineatus to waterborne lead they observed that although the metal caused changes in gill morphology hematocrit remained unaffected. Exposure of rainbow trout toMo failed to upregulate expression of hsp72, hsp73, and hsp90. There was no response in the liver, gills, heart, or erythrocytes of juveniles exposed to a maximum of 20 mg l-1 or in the liver or gills of fingerlings exposed to a maximum of 1000 mg l-1. As a result, there appears to be no utility of these proteins as measures ofMo exposure. There is confidence that the lack of induction in response to acuteMo exposure in trout does not reflect a reduced capacity of fish to activate a heat shock response. In this study, heat shocked fish responded by synthesizing hsp72 and in previous studies that used the same antibodies heat shocked fish responded with inductions in hsp72 and hsp90 in rainbow trout liver, heart, and erythrocytes. Heat shock in rainbow trout has also lead to increases in hsp70 mRNA in the liver, gills, heart, and blood. The lack of hsp induction byMo is also not due to metal load sequestering by MT because, as discussed later, there was no induction of MT in response to Mo exposure. Molybdenum is not the only stressor that is incapable of stimulating hsp70 production. Neither anesthesia administration nor handling induced hsp70 levels in the liver, gills, heart, or muscle of rainbow trout.