Universidade Estadual Paulista, UNESP, Centro de Aquicultura, Via de Acesso Paulo Donato Castellane, 14.884-900, Jaboticabal, SP, Brazil.
Universidade Estadual de Londrina, UEL, Departamento de Ciências Fisiológicas, Rodovia Celso Garcia Cid - Pr 445 Km 380, Campus Universitário, Londrina, PR, 86057-970, Brazil.
Fish Physiol Biochem. 2021 Aug;47(4):895-905. doi: 10.1007/s10695-021-00940-x. Epub 2021 Mar 31.
Stress is an energy-demanding process, as well as the responses of the innate immune system, that impose a metabolic overload on cellular energy production, which can affect the cellular redox balance, causing oxidative damage. We evaluated the role of stress in the modulation of innate immune and oxidative/antioxidant mechanisms in juvenile pacu exposed to acute and chronic stressors. The experimental period lasted 30 days, and fish (113.7 ± 35.1 g) were fed commercial feed. During this period, half of the fish were not manipulated (Condition A), and the other half were chased with a dip net for 5 min twice a day (Condition C). After the 30-day period, fish from both groups were sampled (baseline sampling), and the remainders (not sampled) were air exposed for 3 min (acute stressor), returned to the tanks, and were sampled again 30 min, 3 h, 6 h, and 24 h after air exposure. We evaluated biomarkers of stress (circulating cortisol and glucose), the innate immune system (respiratory burst activity/RBA, hemolytic activity of the complement system (HA-AP) and serum concentration of lysozyme), oxidative damage (lipid peroxidation/LPO), and antioxidant enzymes (superoxide dismutase, SOD; catalase, CAT; and glutathione peroxidase, GSH-Px). Our results showed that stress, acutely or chronically, caused a transient reduction of RAL and activated the HA-AP. Acutely, stress increased the lysozyme concentration. Furthermore, both conditions caused oxidative stress in the liver, and differently they modulated the antioxidant system, enhancing SOD activity and impairing CAT and GSH-Px activity.
应激是一个能量消耗过程,也是先天免疫系统的反应,这会对细胞能量产生造成代谢过载,从而影响细胞氧化还原平衡,导致氧化损伤。我们评估了应激在调节幼期淡水白鲳先天免疫和氧化/抗氧化机制中的作用,这些鱼暴露于急性和慢性应激源下。实验期持续 30 天,鱼(113.7 ± 35.1 g)喂食商业饲料。在此期间,一半的鱼不受干扰(条件 A),另一半用抄网每天追逐两次 5 分钟(条件 C)。30 天后,从两组鱼中取样(基线采样),其余(未采样)鱼暴露在空气中 3 分钟(急性应激源),放回水箱,然后在空气暴露后 30 分钟、3 小时、6 小时和 24 小时再次取样。我们评估了应激生物标志物(循环皮质醇和葡萄糖)、先天免疫系统(呼吸爆发活性/RBA、补体系统的溶血活性(HA-AP)和血清溶菌酶浓度)、氧化损伤(脂质过氧化/LPO)和抗氧化酶(超氧化物歧化酶,SOD;过氧化氢酶,CAT;谷胱甘肽过氧化物酶,GSH-Px)。我们的结果表明,急性或慢性应激会导致 RAL 短暂降低并激活 HA-AP。急性应激会增加溶菌酶浓度。此外,两种条件都会导致肝脏氧化应激,并且它们以不同的方式调节抗氧化系统,增强 SOD 活性并损害 CAT 和 GSH-Px 活性。