Although substantial knowledge of mercury toxicity in fish has been assembled; until now, studies investigating the toxic impacts in Nile tilapia (Oreochromis niloticus) following dietary exposure to organic methyl mercury (MeHg) are less prolific. Accordingly, the current study aimed to evaluate the impacts of MeHg on neurobehavioral and immune integrity in Nile tilapia after dietary exposure. Two hundred and twenty-five juvenile Nile tilapia (19.99 ± 0.33 g) were allocated into five groups in triplicates (15 fish/replicate). G1, G2, G3, G4, and G5. O. niloticus were fed corresponding basal diets containing 0, 0.5, 1, 1.5, and 2 mg/kg diet MeHg chloride (MeHgCl) daily for 30 days, zero value represented the control G1 group. The results showed that MeHg induced significant alterations in O. niloticus behavior, the swimming behavior was significantly decreased, while scratching, biting, and fin tugging behaviors were significantly augmented. Moreover; chasing, mouth pushing, and butting behaviors were significantly increased in all the exposed groups. MeHg significantly decreased brain acetylcholine esterase (AChE) and serum immunoglobulin M (IgM) levels in all the exposed groups. Meanwhile, serum levels of lysozyme (LYZ), nitric oxide (NO), superoxide dismutase (SOD) malondialdehyde (MDA), protein carbonyl (PCO), and 8 hydroxy 2 deoxyguanosine (8OH2dG) were significantly elevated in all the exposed groups except for serum reduced glutathione (GSH) content was significantly decreased implying oxidative stress (OS), lipid peroxidation (LPO), protein, DNA damage and impaired immune response of the exposed tilapia. MeHg significantly altered transcriptional expression of immune-related genes including (TNF-α, IL-1β, and IL-8, and IL-10) in all the exposed groups. From the obtained outcomes, the present research is the premier to investigate that dietary MeHg exposure in O. niloticus significantly induced neurobehavioral and immune defense impairments in a dose-related manner. This study exhibits that dietary MeHg may pose a potential threat to the O. niloticus populations.

尽管已经掌握了鱼类中汞毒性的大量知识；到目前为止，有关饮食中有机甲基汞（MeHg）暴露后对尼罗罗非鱼（Oreochromis niloticus）的毒性影响的研究较少。因此，目前的研究旨在评估甲基汞对饮食接触后尼罗罗非鱼神经行为和免疫完整性的影响。将225个尼罗罗非鱼幼鱼（19.99±0.33 g）分成五组，一式三份（每条鱼15条）。G1，G2，G3，G4和G5。尼罗罗非鱼每天分别喂食含有0、0.5、1、1.5和2 mg / kg日粮MeHg氯化物（MeHgCl）的基础日粮，持续30天，零值代表对照组G1组。结果表明，MeHg诱导了尼罗罗非鱼的显着变化行为，游泳行为显着降低，而抓挠，咬伤和拖尾的行为显着增强。此外; 在所有暴露人群中，追逐，推嘴和对接行为均显着增加。MeHg显着降低所有暴露组的脑乙酰胆碱酯酶（AChE）和血清免疫球蛋白M（IgM）水平。同时，除暴露组外，所有暴露组的血清溶菌酶（LYZ），一氧化氮（NO），超氧化物歧化酶（SOD），丙二醛（MDA），蛋白羰基（PCO）和8羟基2脱氧鸟苷（8OH2dG）均显着升高。血清降低的谷胱甘肽（GSH）含量显着降低，这意味着暴露的罗非鱼的氧化应激（OS），脂质过氧化（LPO），蛋白质，DNA损伤和免疫反应受损。（TNF-α，IL-1β，和IL-8和IL-10）中的所有暴露的基团。从获得的结果来看，本研究是主要的研究，即饮食中甲基汞对尼罗罗非鱼的暴露以剂量相关的方式显着诱导了神经行为和免疫防御障碍。这项研究表明，饮食中的甲基汞可能对尼罗罗非鱼种群构成潜在威胁。