Chronic hypoxia and Cu2+ exposure induce gill remodeling of largemouth bass through endoplasmic reticulum stress, mitochondrial damage and apoptosis.

Hypoxia and Cu2+ pollution often occur simultaneously in aquatic ecosystems and jointly affect physiology of fish. As the respiratory and ion exchange tissue of fish, how gill responds to the stress induced by these two abiotic environmental factors is still unclear. We have conducted a study by exposing largemouth bass (Micropterus salmoides) to hypoxia (2.0 mg·L-1) and/or Cu2+ (0.5 mg·L-1) for 28 days to answer this question. We subsequently studied respiratory rate, Cu2+ transport, endoplasmic reticulum (ER) stress, mitochondrial damage, and morphology in gill tissue on day 7, 14, 21 and 28. We found that hypoxia exposure increased the respiratory rate of largemouth bass, reflecting the response of largemouth bass to cope with hypoxia. Of note, Cu2+ entered gill by specifically binding to CTR1 and its accumulation dramatically in gill disrupted the response of largemouth bass to hypoxia. Hypoxia and/or Cu2+ exposure led to ER stress and mitochondrial damage in gills of largemouth bass. ER stress and mitochondrial damage induced apoptosis by activating caspase-8 and caspase-9 signaling pathways, respectively. Apoptosis induced by hypoxia and Cu2+ exposure had a positive and synergistic effect on gill remodeling by reducing interlamellar cell masses. In addition, Cu2+ exposure induced hypoxia-like remodeling to gill morphology through mechanisms similar to hypoxia exposure. Most of gene expression changed mainly within 21 days and recovered to the control level on day 28, reflecting the acclimation of largemouth bass to hypoxia and/or Cu2+ exposure at gene expression level. Overall, our research suggests that chronic hypoxia and Cu2+ exposure could induce gill remodeling of largemouth bass through ER stress, mitochondrial damage and apoptosis. The outcomes could provide an insight for fish environmental adaptation and environmental toxicology.

Enhance energy supply of largemouth bass (Micropterus salmoides) in gills during acute hypoxia exposure.

Gills are the location of gas exchange and also the first target organ of fish response for environmental stress. As a multifunctional organ, its energy supply, when faced with insufficient dissolved oxygen in the water, remains unclear. In this study, largemouth bass was subjected to hypoxia stress (1.2 mg/L) for 24 h and 12 h reoxygenation (R12) to evaluate energy supply strategy of gills. Under hypoxia exposure, the respiratory rate of largemouth bass increased by an average of 20 breaths per minute. A total of 2026, 1744, 1003, 579, 485, and 265 differentially expressed genes (DGEs) were identified at 0 h, 4 h, 8 h, 12 h, 24 h, and R12h in gills after hypoxia exposure. KEGG functional analysis of DEGs revealed that the glycolysis/gluconeogenesis pathway was enriched across all the sampling points (0, 4, 8, 12, 24 h, R12). The gene expression and enzyme activity of three rate-limiting enzymes (hexokinase, phosphofructokinase-6, pyruvate kinase) in glycolysis pathway were significantly increased. Increased levels of glycolysis products pyruvate and lactic acid, as well as the number of mitochondria (1.8-fold), suggesting an enhancement of aerobic and anaerobic metabolism of glucose in gills. These results suggest that the gill of largemouth bass enhanced the energy supply during acute exposure to hypoxia stress.

The relationship between childhood trauma and Internet gaming disorder among college students: A structural equation model.

BACKGROUND: The aim of this study was to investigate the mechanisms of Internet gaming disorder (IGD) and the associated interaction effects of childhood trauma, depression and anxiety in college students. METHODS: Participants were enrolled full-time as freshmen at a University in the Hunan province, China. All participants reported their socio-demographic characteristics and undertook a standardized assessment on childhood trauma, anxiety, depression and IGD. The effect of childhood trauma on university students' internet gaming behaviour mediated by anxiety and depression was analysed using structural equation modelling (SEM) using R 3.6.1. RESULTS: In total, 922 freshmen participated in the study, with an approximately even male-to-female ratio. A mediation model with anxiety and depression as the mediators between childhood trauma and internet gaming behaviour allowing anxiety and depression to be correlated was tested using SEM. The SEM analysis revealed that a standardised total effect of childhood trauma on Internet gaming was 0.18, (Z = 5.60, 95% CI [0.02, 0.05], P < 0.001), with the direct effects of childhood trauma on Internet gaming being 0.11 (Z = 3.41, 95% CI [0.01, 0.03], P = 0.001), and the indirect effects being 0.02 (Z = 2.32, 95% CI [0.00, 0.01], P = 0.020) in the pathway of childhood trauma-depression-internet gaming; and 0.05 (Z = 3.67, 95% CI [0.00, 0.02], P < 0.001) in the pathway of childhood trauma-anxiety-Internet gaming. In addition, the two mediators anxiety and depression were significantly correlated (r = 0.50, Z = 13.54, 95% CI [3.50, 5.05], P < 0.001). CONCLUSIONS: The study revealed that childhood trauma had a significant impact on adolescents' Internet gaming behaviours among college students. Anxiety and depression both significantly mediated the relationship between childhood trauma and internet gaming and augmented its negative influence. Discussion of the need to understand the subtypes of childhood traumatic experience in relationship to addictive behaviours is included.