Coping strategies in response to different levels of elevated water hardness in channel catfish (Ictalurus punctatus): Insight into ion-regulatory and histopathological modulations

Abstract

Water hardness above the optimal level can incite toxic effects in fish, which are often species specific. Hence, we aimed at obtaining insights on the potential effects of elevated water hardness as well as coping strategies in channel catfish (Ictalurus punctatus). First, a toxicity assay was performed where the 96 h-LC₅₀ was calculated as 4939 mg/L CaCO₃. Thereafter, to gain knowledge on the underlying adaptive strategies to high water hardness, fish were exposed to seven hardness levels (150, 600, 1000, 1500, 2000, 3000 and 4000 mg/L CaCO₃ at pH 8.15) for 15 days. Results showed that branchial activities of Ca²⁺-ATPase and Na⁺/K^+-ATPase, which facilitate Ca²⁺ uptake, reduced starting respectively from 1000 mg/L and 1500 mg/L CaCO₃. Nevertheless, Ca²⁺ burden in plasma and tissue (gills, liver and intestine) remained elevated. Hardness exposure also disturbed cations (Na⁺, K⁺, Mg²⁺) and minerals (iron and phosphorus) homeostasis in a tissue-specific and dose-dependent manner. Both hemoglobin content and hematocrit dropped significantly at 3000-4000 mg/L CaCO₃, with a parallel decline in iron content in plasma and gills. Muscle water content rose dramatically at 4000 mg/L CaCO₃, indicating an osmo-regulation disruption. Higher hardness of 3000-4000 mg/L CaCO₃ also incited a series of histopathological modifications in gills, liver and intestine; most likely due to excess Ca²⁺ accumulation. Overall, these data suggest that channel catfish can adapt to a wide range of elevated hardness by modulating Ca²⁺ regulatory pathways and histomorphological alterations, however, 1500 mg/L CaCO₃ and above can impair the performance of this species.

Keywords: Aquaculture; Histopathology; Ion transporters; Ion-osmoregulation; Lethal toxicity; Water hardness.