Miswak (Salvadora persica) modulated the growth performance, antioxidative response, and histopathological damage induced by zinc toxicity in Nile tilapia (Oreochromis niloticus).

Abstract

In this study, Nile tilapia fingerlings with average body weight (8.6 ± 0.06 g) were exposed to zinc (Zn) toxicity and tested its amelioration with miswak (Salvadora persica L.) (SP) supplemented diet. Five fish groups were fed on diets with SP at 0, 0.25, 0.5, 1.0, and 2.0% (T1, T2, T3, T4, and T5, respectively) diet without Zn exposure, while another five groups were exposed to Zn at 7 mg/L and co-supplemented with SP at 0, 0.25, 0.5, 1.0, and 2.0 % (T6, T7, T8, T9, and T10, respectively). After 12 weeks, fish-fed 1.0% SP diet (T4) achieved the highest growth and feed performances, while the lowest one was in Zn-exposed fish (T6) (P < 0.05). T6 and T7 groups showed the most inferior carcass protein and ash contents, while T4 and T5 showed the highest lipid content (P < 0.05). The level of Zn residue increased in fish exposed to Zn (P < 0.05). Fish exposed to Zn and fed SP showed high blood urea, catalase, ALT, AST, and total superoxide dismutase (T-SOD), while the malondialdehyde (MDA) was decreased (P < 0.05). Interestingly, miswak resulted in elevated catalase and T-SOD and reduced MDA in fish without Zn exposure (P < 0.05). Zn exposure causes abnormal histopathological characteristics in gills, hepatopancreas, posterior kidney, and musculature tissues of tilapia, while fish-fed SP showed regular, healthy, and protected histopathological characters. The results suggested that SP can induce the antioxidant responses that prepare Nile tilapia for a further suppressive oxidative condition (i.e., Zn exposure).