BACKGROUND: Heavy metal pollution, particularly lead (Pb), poses a significant threat to aquatic ecosystems and their inhabitants, threatening their delicate balance and long-term viability. This study highlights the urgent need to mitigate heavy metal pollution in aquatic ecosystems.
OBJECTIVE: This study investigates Pb(NO3)2 exposure effects on tissue accumulation, behavioral abnormalities, and hemato-biochemical parameters in common carp (Cyprinus carpio), a widely distributed freshwater fish species.
METHODS: Fish (115 ± 5.23 g) were exposed to various Pb(NO3)2 concentrations for 10 and 20 days, representing control (0 %), 25 %, 50 %, and 75 % of the LC50 equivalent to 19.33, 38.66, and 58.0 mg/l, respectively. The standard manual procedure was used for blood sampling. The lead concentration in fish tissue was determined using an atomic absorption spectrophotometer.
RESULTS: Results revealed that fish gills showed significant (P < 0.05) increase in Pb(NO3)2 after 10 days, further rising after 20 days. Liver concentrations also rose significantly (P < 0.05) with prolonged exposure and increasing Pb levels. Muscle had lower concentrations. Hematological parameters (RBC, WBC, HB, HCT) decreased with higher Pb(NO3)2 levels. Behavioral and morphological changes were significantly more pronounced in the exposure groups when compared to the control group. Hepatic enzyme activities (AST, ALT), glucose, and lipid levels increased, while total protein decreased.
CONCLUSIONS: The study highlights Pb(NO3)2 harmful effects on common carp, impacting tissue accumulation, hematological parameters, and biochemical disruptions. It emphasizes the need to monitor and mitigate heavy metal pollution in aquatic environments to safeguard freshwater organisms and ecosystems, and to further increase our understanding of Pb toxicity in freshwater ecosystems.

Mitochondrial function can be regulated by ion channels. Mitochondrial RNA splicing 2 (Mrs2) is a magnesium ion (Mg2+) channel located in the inner mitochondrial membrane, thereby mediating the Mg2+ influx into the mitochondrial matrix. However, its potential role in regulating the Mg homeostasis and mitochondrial function in aquatic species is still unclear. This study molecularly characterizes the gene encoding Mrs2 in fish M. amblycephala with its functions in maintaining the Mg homeostasis and mitochondrial function verified. The mrs2 gene is 2133 bp long incorporating a 1269 bp open reading frame, which encodes 422 amino acids. The Mrs2 protein includes two transmembrane domains and a conserved tripeptide Gly-Met-Asn, and has a high homology (65.92-97.64%) with those of most vertebrates. The transcript of mrs2 was relatively high in the white muscle, liver and kidney. The inhibition of mrs2 reduces the expressions of Mg2+ influx/efflux-related proteins, mitochondrial Mg content, and the activities of mitochondrial complex I and V in hepatocytes. However, the over-expression of mrs2 increases the expressions of Mg2+ influx/efflux-related proteins, mitochondrial Mg content, and the complex V activity, but decreases the activities of mitochondrial complex III and IV and citrate synthase in hepatocytes. Collectively, Mrs2 is highly conserved among different species, and is prerequisite for maintaining Mg homeostasis and mitochondrial function in fish.

The widespread application of herbicides raises concerns about their impact on non-target aquatic organisms. This study aimed to evaluate the toxicity of a commercially available herbicide formulation containing Bromoxynil+MCPA (2-Methyl-4-chlorophenoxyacetic acid) on Cirrhinus mrigala (economically significant fish). A total of 210 juvenile fish were subjected to a triplicate experimental setup, with 70 fish allocated to each replicate, exposed to seven different concentrations of herbicide: 0 mg/L, 0.133 mg/L, 0.266 mg/L, 0.4 mg/L, 0.5 mg/L, 0.66 mg/L, and 0.8 mg/L, respectively, for a duration of 96 h. The median lethal concentration (LC50) was determined to be 0.4 mg/L. Significant hematological alterations were observed, including decreases in RBC counts, hemoglobin, hematocrit, and lymphocyte counts, along with an increase in erythrocyte indices. Biochemical analysis revealed elevated levels of neutrophils, WBCs, bilirubin, urea, creatinine, ALT, AST, ALP, and glucose in treated groups. Morphological abnormalities in erythrocytes and histopathological changes in gills, liver, and kidneys were noted. Pathological alterations in gills, liver and kidneys including epithelial cell uplifting, lamellar fusion, hepatolysis, and renal tubule degeneration were observed. Oxidative stress biomarkers such as TBARS (Thiobarbituric Acid Reactive Substance), ROS (Reactive Oxygen Species), and POD (Peroxides) activity increased, while antioxidant enzymatic activities decreased as toxicant doses increased from low to high concentrations. The study reveals that Bromoxynil+MCPA significantly disrupts physiological and hematobiochemical parameters in Cirrhinus mrigala, which highlights the substantial aquatic risks. In conclusion, the herbicide formulation induced significant alterations in various fish biomarkers, emphasizing their pivotal role in assessing the environmental impact of toxicity. This multi-biomarker approach offers valuable insights regarding the toxicological effects, thereby contributing substantially to the comprehensive evaluation of environmental hazards.

Dynamin-related protein 1 (DRP1) is a key regulator in the maintenance of mammalian glucose homeostasis, but the relevant information remains poorly understood on aquatic animals. In the study, DRP1 is formally described for the first time in Oreochromis niloticus. DRP1 encodes a peptide of 673 amino acid residues that contained three conserved domains: a GTPase domain, a dynamin middle domain and a dynamin GTPase effector domain. DRP1 transcripts are widely distributed in all of the detected seven organs/tissues, and the highest mRNA levels in brain. High-carbohydrate (45 %) fed fish showed a significant upregulation of liver DRP1 expression than that of control (30 %) group. Glucose administration upregulated liver DRP1 expression, with peak values observed at 1 h; then its expression returned to the basal value at 12 h. In the in vitro study, DRP1 over-expression significantly decreased mitochondrial abundance in hepatocytes. DHA significantly increased mitochondrial abundance, transcriptions of mitochondrial transcription factor A (TFAM) and mitofusin 1 and 2 (MFN1 and MFN2) and complex II and III activities of high glucose-treated hepatocyte, whereas the opposite was true for DRP1, mitochondrial fission factor (MFF) and fission (FIS) expression. Together, these findings illustrated that O. niloticus DRP1 is highly conserved, and it participated in glucose control of fish. DHA could alleviate high glucose-induced mitochondrial dysfunction of fish by inhibiting DRP1-mediated mitochondrial fission.

Carbonylcyanide-3-chlorophenylhydrazone (CCCP) is a protonophore, which causes uncoupling of proton gradient in the inner mitochondrial membrane, thus inhibiting the rate of ATP synthesis. However, this information is manly derived from mammals, while its effects on the mitochondrial homeostasis of aquatic animals are largely unknown. In this study, the mitochondrial homeostasis of a carp fish Megalobrama amblycephala was investigated systematically in a time-course manner by using CCCP. Fish was injected intraperitoneally with CCCP (1.8 mg/kg per body weight) and DMSO (control), respectively. The results showed that CCCP treatment induced hepatic mitochondrial oxidative stress, as was evidenced by the significantly increased MDA and PC contents coupled with the decreased SOD and MnSOD activities. Meanwhile, mitochondrial fission was up-regulated remarkably characterized by the increased transcriptions of Drp-1, Fis-1 and Mff. However, the opposite was true for mitochondrial fusion, as was indicative of the decreased transcriptions of Mfn-1, Mfn-2 and Opa-1. This consequently triggered mitophagy, as was supported by the accumulated mitochondrial autophagosomes and the increased protein levels of PINK1, Parkin, LC3-II and P62 accompanied by the increased LC3-II/LC3-I ratio. Mitochondrial biogenesis and function both decreased significantly addressed by the decreased activities of CS, SDH and complex I, IV and V, as well as the protein levels of PGC-1β coupled with the decreased transcriptions of TFAM, COX-1, COX-2 and ATP-6. Unlikely, DMSO treatment exerted little influence. Overall, CCCP treatment resulted in the imbalance of mitochondrial homeostasis in Megalobrama amblycephala by promoting mitochondrial oxidative stress, fission and mitophagy, but depressing mitochondrial fusion, biogenesis and function.

More and more frequently these days, aquatic ecosystems are being stressed by nutrient enrichment, pollutants, and global warming, leading to a serious depletion in oxygen concentrations. Although a sudden, significant lack of oxygen will result in mortality, fishes can have an acute behavior (e.g., an increase in breathing rate, reduction in swimming frequency) and physiology responses (e.g., increase in oxygen delivery, and reduction in oxygen consumption) to hypoxia, which allows them to maintain normal physical activity. Therefore, in order to shed further light on the molecular mechanisms of hypoxia adaptation in fishes, the authors conduct comparative quantitative proteomics on Pelteobagrus vachelli livers using iTRAQ. The research identifies 511 acute hypoxia-responsive proteins in P. vachelli. Furthermore, comparison of several of the diverse key pathways studied (e.g., peroxisome pathway, PPAR signaling pathway, lipid metabolism, glycolysis/gluco-neogenesis, and amino acid metabolism) help to articulate the different mechanisms involved in the hypoxia response of P. vachelli. Data from proteome analysis shows that P. vachelli can have an acute reaction to hypoxia, including detoxification of metabolic by-products and oxidative stress in light of continued metabolic activity (e.g., peroxisomes), an activation in the capacity of catabolism to get more energy (e.g., lipolysis and amino acid catabolism), a depression in the capacity of biosynthesis to reduce energy consumption (e.g., biosynthesis of amino acids and lipids), and a shift in the aerobic and anaerobic contributions to total metabolism. The observed hypoxia-related changes in the liver proteome of the fish can help to understand or can be related to the hypoxia-related response that takes place in similar conditions in the liver or other proteomes of mammals.