Implications of deltamethrin on hematology, cardiac pathology, and gene expression in Nile tilapia (Oreochromis niloticus) and its possible amelioration with Shatavari (Asparagus racemosus).

Abstract

Deltamethrin (DM) is one of the extensively used pyrethroids for controlling ectoparasites. Unfortunately, DM is highly toxic to fish as it primarily targets the sodium channels of the plasma membrane thereby affecting their cardiac and nervous systems. The present study investigated the protective efficacy of Shatavari (Asparagus racemosus) against DM-induced cardiotoxicity in Nile tilapia (Oreochromis niloticus). The fish were segregated into nine groups having 36 fish/group maintained in triplicates exposed to DM (1µg/L) and fed with a diet containing three different concentrations (10g, 20g, and 30g/kg feed) of aqueous extract of A. racemosus (ARE) for 21 days. DM caused significant alterations in the blood and serum parameters, and expression of cardiac and apoptotic genes compared to the control group. The ARE cotreatment significantly reduced the increase in serum transaminases, creatine kinase, and lactate dehydrogenase levels induced by DM. ARE facilitated the regain of electrolyte (sodium, potassium, chloride) homeostasis and antioxidants such as catalase, superoxide dismutase, glutathione peroxidase, and glutathione in DM-exposed fish. The cardiac histology exhibited loose separation of the cardiomyocytes and myofibrillar loss in the DM group which was ameliorated in the DM-ARE cotreatment group. Significant modulations were observed in the expression of cardiac-specific genes (gata4, myh6, tnT, cox1) and apoptosis signaling genes and proteins (HSP70, bax, bcl-2, caspase3), in the cotreatment group compared to the DM-exposed group. The current study suggests that ARE possesses potential cardioprotective properties that are effective in mitigating the toxic effects induced by DM via ameliorating oxidative stress, electrolyte imbalance, and apoptosis in tilapia.