Gill epithelial responses of Cyprinus carpio Linnaeus, 1758 as sensitive histological biomarkers of sublethal anthropogenic stress in the Ile River (Kazakhstan)

Reactivity of Gill and Intestinal Mucosal Barriers in Common Bream (Abramis brama): A Comparative Histological and Ultrastructural Study of Natural Populations

Fish mucosal barriers are sensitive interfaces between the organism and the aquatic environment and may reflect integrated tissue responses in natural populations. This study assessed the reactivity of the gill and intestinal mucosal barriers in common bream, Abramis brama, from the Ile–Balkhash Basin and Lake Alakol, Kazakhstan. A total of 50 individuals were examined using light microscopy, transmission electron microscopy, quantitative cell counting, and semi-quantitative histopathological assessment. Background hydrochemical parameters of the studied waters were within guideline values and were used as environmental context rather than as a control condition for tissue normality. Histopathological alterations were recorded in both organs. The gills showed epithelial desquamation, respiratory epithelial edema, deformation and fusion of secondary lamellae, epithelial hyperplasia, and vascular abnormalities, with a median Gill Lesion Score of 2.00 (IQR 1.86–2.29). The intestine showed epithelial sloughing, intestinal fold disruption, brush-border damage, cellular infiltration, fibrosis/collagenization, and vascular changes, with a median Intestinal Lesion Score of 2.14 (IQR 1.86–2.57). Rodlet cells were more abundant in the gills, whereas mast/eosinophilic granular cells occurred at comparable densities in both organs. These findings indicate shared but organ-specific patterns of mucosal reactivity and support paired gill–intestine analysis as an informative morphological approach for assessing wild fish populations under natural multifactorial conditions.

Thirty weeks exposure reveals the damaging effects of microplastics: Histology, immunity and intestinal microbiota of grass carp (Ctenopharyngodon idella).

Microplastic (MP) pollution has become a global aquatic environmental issue, yet its long-term toxic effects on aquatic organisms remain poorly understood. In this study, grass carps (Ctenopharyngodon idella) were subjected to thirty weeks dietary exposure to polystyrene microplastics (PS-MPs) to systematically evaluate the effects on histology, immune signaling, and intestinal microbiota. Histopathological examination revealed that PS-MPs exposure induced focal necrosis, increased melanomacrophage centers, and sinusoidal congestion in the spleen, while the intestine exhibited villus fusion, disordered arrangement, epithelial edema, and lymphocyte infiltration. Transcriptomic analysis further identified 2975 differentially expressed genes (DEGs) in the spleen. Functional enrichment analysis revealed that these DEGs were significantly associated with cytokine-cytokine receptor interaction, Toll-like receptor, RIG-I-like receptor, and NOD-like receptor signaling pathways. Notably, the MAPK-associated gene mapkapk3 was significantly upregulated, whereas the immune-regulatory receptor gene IL20RA was downregulated, suggesting disruption of immune homeostasis and remodeling of innate immune signaling. Gut microbiota analysis revealed marked dysbiosis characterized by increased relative abundances of Fusobacteriota (57%) and Proteobacteria (35%), accompanied by pronounced reductions in Bacteroidota and Firmicutes. All alpha diversity indices (Chao1, Ace, Shannon, Simpson) were significantly decreased, and beta diversity analyses (PCA, PCoA, NMDS) demonstrated clear separation between groups. The opportunistic pathogen Aeromonas veronii was significantly enriched and identified as a key biomarker in the PS-MPs group. Collectively, long-term PS-MPs exposure induced structural tissue damage, altered immune-related transcriptional profiles involving mapkapk3 and IL20RA, and promoted gut microbial dysbiosis with enrichment of opportunistic pathogens, thereby potentially increasing host susceptibility to environmental stressors. These findings provide mechanistic insight into the ecological health risks posed by chronic MP exposure in freshwater fish.

Integrated histopathological, physiological, biochemical, and molecular analysis of gill responses to acute salinity stress in red tilapia (Oreochromis spp.)

Growing freshwater scarcity in China is driving aquaculture interests toward saline‐tolerant fish species. Red tilapia (Oreochromis spp.) is a euryhaline species with strong osmoregulatory capacity, making it an ideal model for investigating stress‐induced physiological changes. In this study, we examined the gill responses of red tilapia subjected to acute salinity stress. Fish were maintained in either (0 h, Ctrl group) or saline water (17.7‰ ± 0.1‰) for 192 h; time points (0, 24, 48, 96, 192 h). Gill samples were collected over a time course for integrated histopathological and physiological analyses. Exposure to saline water induced histopathological alterations, including lamellar shortening and thickening, as well as a significant increase in the apoptotic index. Using qRT‐PCR, we confirmed the significant activation in gills under salinity stress of genes associated with apoptosis (tnfsf1, birc5a, casp6, ddit3), ABC transporters (cftr, tap1), and Toll‐like receptor (TLR) signaling (irak1, nfkbiaa). These molecular responses reflect three key processes: osmoregulation (ABC transporters), immune and inflammatory regulation (TLR signaling), and cell fate control (apoptosis). Collectively, they underpin the disruption of homeostasis, immune activation, and oxidative stress observed during acute salinity exposure. Biochemical profiling revealed a dynamic osmoregulatory response: early upregulation of Na+/K+‐ATPase, NKCC1, and antioxidant enzymes (SOD, CAT, GSH‐Px) was followed by a late‐stage oxidative imbalance, characterized by sustained elevation of malondialdehyde (MDA) and reduced antioxidant capacity. Ion homeostasis became progressively disrupted, with significant alterations in Na+ and Cl− levels. Molecular analysis further uncovered a coordinated transcriptional sequence: an initial anti‐apoptotic phase, succeeded by delayed upregulation of pro‐apoptotic and immune‐related pathways (including IgM and LZM), occurring alongside modulation of osmoregulatory genes. Together, these findings provide a mechanistic basis for understanding salinity adaptation in red tilapia.

Effects of atrazine on tissue damage, physiological and biochemical changes and transcriptome in marine medaka (Oryzias melastigma).

Atrazine (ATZ), a widely used triazine herbicide frequently detected in aquatic environments, poses ecological risks, yet its toxicity mechanisms in estuarine/marine organisms remain unclear. The present study employed juvenile Oryzias melastigma (marine medaka) as the model organism, and the 96-h median lethal concentration (LC50) of ATZ was determined to be 31.65 mg/L. Juvenile marine medaka were exposed to 0, 0.09, 0.36, 1.07, and 3.28 mg/L ATZ for 30 days. Histopathology revealed severe gill alterations (hyperplasia, apical enlargement, disintegration of the lamellae and filament congestion) and hepatic injuries (sinusoidal dilation, cytoplasmic vacuolization, acidophilic body formation and nuclear pyknosis). Biochemically, ATZ altered Na+-K+-ATPase and Ca2+-ATPase activities in the gills, reduced the activity of catalase (CAT) in the liver. ATZ at concentrations of 0.09 and 0.36 mg/L could markedly decrease the activity of total superoxide dismutase (T-SOD), and increase the malondialdehyde (MDA) content in medaka liver. Additionally, ATZ exposure upregulated the expression levels of ucp-2 and decreased the expression levels of cox-2, ccl20, il-1β, cat and sod. Transcriptome results showed 1,078 differentially expressed genes (DEGs) in the liver, with 436 upregulated and 642 downregulated DEGs. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that ATZ exposure disturbed the expression of genes associated with the HIF-1 and PI3K-Akt signaling pathways, suggesting that ATZ may induce hypoxia, oxidative damage and apoptosis. These results corroborate the histological and enzymatic evidence, providing insights into the toxicological impacts and mechanisms of chronic ATZ exposure in estuarine and marine fish.

Determination of microplastic-mediated oxidative stress responses and DNA damage in economically important fish species in the largest dam lakes (Keban, Karakaya, and Atatürk) of Türkiye

Mechanistic Insights Into Aflatoxin B1-Induced Histopathology in the Gill, Liver, and Kidney Tissues and Immune Dysregulation by Altering the Expression of Cytokine Genes in Channa punctata.

Aflatoxin B1 (AFB1) is one of the most potent mycotoxins and poses substantial health concerns to humans and other animals, including aquatic organisms. Addressing the increasing AFB1 contamination in aquaculture due to the utilization of plant-based ingredients for aquafeed formulations. In this study, we investigated the impact of sublethal doses of Aflatoxin B1 (11.4, 22.8, and 45.5 μg) on the multiple tissue histology and hepatic cytokine gene expression in Channa punctata after 28 days of exposure. Dose-dependent histological alterations were seen in the gill, liver, and kidney tissues. Gill tissues exhibited epithelial lifting, hyperplasia, lamellar fusion, and shortening of secondary lamellae. Liver sections showed hepatic tissue alterations, including cytoplasmic vacuolation, congestion, and necrosis, particularly at medium and high doses. Renal tissue displayed glomerular atrophy, hyperplasia in the Bowman's capsule, and tubular necrosis. Furthermore, AFB1 exposure modulated hepatic cytokine gene expression. At a low AFB1 concentration, a significant upregulation of both pro-inflammatory (TNF-α, INF-γ, and IL-6) and anti-inflammatory (IL-10) cytokine expression was observed, suggesting a regulatory inflammatory response. As the concentration was increased, the anti-inflammatory cytokine mRNA expression was downregulated, indicating immunotoxic stress. Overall, the study suggests that AFB1 induces multiorgan histopathology and also immune dysregulation by modulating the hepatic cytokine gene expression. To our best knowledge, this research draft may represent one of the earliest findings that provide comprehensive evidence of multiorgan histopathology and immune alterations induced by AFB1 in Channa punctata.