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This study aimed to understand the effects of freshwater acidification, driven by industrial runoff, agricultural activities, and atmospheric deposition, on the freshwater mollusk Bellamya bengalensis. By systematically investigating the impact of two common carboxylic acids, acetic acid (AA) and benzoic acid (BA), this research employed diverse toxicological, pathological, and ecological assessments. We explored survival predictions through the generic unified threshold model of survival (GUTS-SD), examined oxidative stress responses, and investigated hepatopancreatic alterations. In the experimental design, Bellamya bengalensis were subjected to environmentally relevant sublethal concentrations (10%, 20% LC50) of AA (39.77 and 79.54 mg/l) and BA (31.41 and 62.82 mg/l) over 28 days. Acute toxicity tests revealed increased LC50 values, indicating heightened toxicity with prolonged exposure, particularly due to the greater potency of benzoic acid compared to acetic acid. The GUTS-SD model provided accurate predictions of time-specific effects on populations, presenting long-term exposure (100 days) LC50 values for AA (263.7 mg/l) and BA (330.9 mg/l). Sequentially, the integrated biomarker response (IBR) analysis across study intervals highlighted the 28-day interval as the most sensitive, with GST emerging as the most responsive enzyme to oxidative stress induced by AA and BA. Histopathological and ultrastructural assessments of the hepatopancreas showed severe alterations, including necrosis, vacuolation and disrupted micro-villi, which were especially pronounced in higher BA exposure concentrations. These findings highlight the health and survival impacts of carboxylic acid toxicity on Bellamya bengalensis, emphasizing the need for proactive measures to mitigate acidification in aquatic ecosystems. The broader ecological implications underscore the importance of effective management and conservation strategies to address ongoing environmental challenges [Display omitted] • Investigated AA and BA effects on Bellamya bengalensis. • Used GUTS-SD model for survival and LC50 prediction. • Examined hepatopancreas for histopathology and ultrastructure. • Assessed antioxidant enzymes and lipid peroxidation. • Identified distinct AA and BA toxicity mechanisms. [ABSTRACT FROM AUTHOR]

Graphical abstract Syntheses, crystal structures and luminescence behaviors of four neutral penta/hexacoordinate cadmium(II) compounds containing a tridentate (N,N,N) Schiff base are described. X-ray crystallographic study demonstrates that cadmium(II) ion is able to form mono-, di- and polynuclear compounds through judicious choice of halide/pseudohalide ions. In crystalline states, the compounds afford different crystalline architectures. Highlights • Four neutral cadmium(II)halido/pseudohalido compounds with a tridentate Schiff base are isolated. • X-ray structures reveal two pentacoordinated mononuclear halido, one hexacoordinated thiocyanato bridged dinuclear and one azido bridged polynuclear cadmium(II). • In crystalline states, the compounds afford different crystalline architectures. • Thermally stable all compounds exhibit intraligand 1(π-π∗) fluorescence in DMF solutions at room temperature with lifetimes in range 0.83–2.94 ns. Abstract Two neutral pentacoordinate mononuclear cadmium(II) complexes of the type [Cd(L)X 2 ] [L = N-(pyridin-2′-yl)benzylidene)-2-(piperidin-1-yl)ethane-1,2-diamine; X = Cl, (1) and X = Br, (2)], one neutral hexacoordinate dinuclear compound [Cd(L)(µ-NCS)NCS] 2 (3) and one neutral hexacoordinate coordination polymer [Cd(L)(µ-N 3)N 3 ] n (4) have been prepared and characterized using microanalytical, spectroscopic, thermal and X-ray crystallographic results. Structural analyses show that each cadmium(II) center in the isostructural compounds 1 and 2 adopts a distorted square pyramidal geometry with a CdN 3 X 2 [X = Cl in 1 and X = Br in 2 ] chromophore through coordination of three N atoms of L and two terminal halides. In 3 and 4, each metal(II) center affords a distorted octahedral geometry with MN 5 S (in 3) and MN 6 (in 4) chromophores. Each metal(II) center in dinuclear compound 3 is attached to three N -atoms of L, one N -atom of terminal thiocyanate, and one N -atom and one S-atom of two μ 1,3 -bridging thiocyanate units, whereas three N -atoms of L and three N -atoms of one terminal and two μ 1,3 -bridging azide units are bound to each metal(II) center in the coordination polymer 4. Each metal(II) center in 4 is connected to two other metal(II) centers through two different μ 1,3 -azide bridges affording a zigzag one-dimensional (1D) chain. In the crystalline state, mononuclear units in both 1 and 2 are stabilized through intermolecular C H ∙∙∙ X (X = Cl in 1 and X = Br in 2) hydrogen bonds promoting to 2D sheet structures. The dinuclear units in 3 pack through cooperative intermolecular C H ∙∙∙ S and C H ∙∙∙ N hydrogen bonds giving rise to a 3D network structure. 1D chains in 4 are stabilized through cooperative intermolecular C H ∙∙∙ N hydrogen bonds promoting to a 2D sheet structure. These 2D sheets, in turn, self-assemble through weak non-covalent π ∙∙∙ π interactions to afford a 3D network structure. The thermally stable compounds (1 – 4) exhibit intraligand 1(π-π∗) fluorescence in DMF solutions at room temperature with lifetimes in range 0.83–2.94 ns. [ABSTRACT FROM AUTHOR]

The acute toxicity of mercury to the air-breathing fish Clarias batrachus (Linn.) was determined in this study using hematological (including hemoglobin, hematocrit, total erythrocyte count, total leukocyte count, and mean corpuscular hemoglobin concentration) and biochemical (including total serum protein, serum glucose, triglyceride, cholesterol, albumin) biomarkers at predetermined exposure concentrations (0.069 and 0.139 mg/L). Although significant differences were observed between exposure groups for all hematological and biochemical variables, a distinctive reduction in hemoglobin levels, hematocrit, and total erythrocyte count in the mercury-exposed fish compared to the control was observed from 24 h–96 h. Similarly, marked differences in serum globulin, total serum protein and cholesterol levels were observed across exposure groups from 24 h–96 h. While the marked hematological responses strongly suggestive of toxicant-related anemia, the marked biochemical responses suggest immune-modulation and metabolic disruption. The magnitude of toxic effects under graded toxicant exposures for weighted scores of combined biomarker response index (IBR) indicated an approximately 3-fold deterioration in overall health of mercury-exposed fish compared to control group. Depictions of hematological and biochemical effects in hardy species like Clarias batrachus indicate an imminent onset of anemia, immune-modulation and metabolic disruption within 24hs of exposure to inorganic mercury. Such observations for portends greater deleterious effects to less hardy aquatic biota under acute inorganic mercury environmental exposures. [Display omitted] • The acute toxicity of mercury to Clarias batrachus (Linn.) was determined. • Lowered hemoglobin and hematocrit levels in exposed group suggest induced anemia. • Lowered serum globulin in exposed group indicates down-regulation of immune capacity. • Increased cholesterol in the exposed group suggests metabolic disruption. [ABSTRACT FROM AUTHOR]

The toxic effects of Zinc oxide nanoparticles (nZnO) on Branchiura sowerbyi and Heteropneustes fossilis , was assessed in a 96-hour acute exposure regime using behavioral (including loss-of balance and clumping tendencies) and physiological (mucus secretion and oxygen consumption) endpoints. While the relationship between behavioral, physiological biomarkers, and exposure concentrations was assessed using correlation analysis, nZnO toxicity was further predicted using the General Unified Threshold model for Survival (GUTS). The time-dependent lethal limits for acute nZnO toxicity (LC 50) on B. sowerbyi were estimated to be 0.668, 0.588, 0.448, and 0.400 mg/l, respectively, at 24, 48, 72, and 96 h whereas for H. fossilis the LC50 values are 0.954, 0.905, 0.874 and 0.838 mg/l. Threshold effect values i.e., LOEC (Lowest Observed Effect Concentration), NOEC (No Observed Effect Concentration), and MATC (Maximum Acceptable Toxicant Concentration) threshold effect values at 96 h were higher for fish compared to the oligochaete. For B. sowerbyi , the GUTS-SD (stochastic death) model is a better predictor of nanoparticle exposure effects compared to the GUTS-IT (individual tolerance) model, however in the case of H. fossilis , the reverse pattern was observed. Oxygen consumption rate was negatively correlated to mortality under acute exposure duration. The strong negative correlation between mortality and oxygen consumption strongly suggests a metabolic-toxicity pathway for nZnO exposure effects. The higher toxicity threshold values i.e., LOEC, NOEC, and MATC for fish compared to the oligochaete invertebrate indicates greater risks for invertebrates compared to vertebrates, with resultant implications for local habitat trophic relationships. [Display omitted] • Acute zinc oxide nanoparticle sensitivity in catfish and worm was examined. • Behavioral and physiological endpoints were examined. • General Unified Threshold model for Survival (GUTS) was applied to assess nZnO toxicity. • Sublethal nZnO exposure can impact the physiology of fish and fish-food organisms in the wild. [ABSTRACT FROM AUTHOR]

Lipopolysaccharide (LPS) is known to induce inflammation and immunonomodulation in a piscine model of Danio rerio. Present study aimed to explore the ability of melatonin in attenuating LPS-induced oxidative damages using this model. In LPS-exposed fish, activation of stress marker MDA was observed in brain with corresponding augmentation of multiple pro-inflammatory cytokines (IL1β, IL6, IL10 and TNFα). In addition, it also showed marked increase in the levels of heat shock factor (HSF) and heat shock proteins (HSPs) in association with transcription factors (NF-kB and NRF2) and mitogen-activated protein kinases (MAPKs). The changes in the levels of these mediators are highly correlated with the induction of pro-inflammatory cytokines. In melatonin-treated fishes, significant amelioration of oxidative stress was observed with reduced levels of MDA and pro-inflammatory cytokines. Melatonin also modulated expression of HSPs that facilitated the brain to overcome inflammation-induced stress by directly initiating NFkB/NRF2 translocation. In summary, melatonin effectively functions to reduce stress induced inflammatory signalling through modulation of oxidative stress and protects the brain from the neuropathological insult. • Lipopolysaccharide initiates oxidative damage and destabilise antioxidant balance. • Lipopolysaccharide incites acute inflammation and cause cytokine storm in brain tissue. • Lipopolysaccharide persuades caspase-dependent apoptosis in the fish brain. • Melatonin ameliorates neuroinflammation by neutralising generated free radicals. • Melatonin prevents brain damage by modulating molecular chaperons and MAPK signal. [ABSTRACT FROM AUTHOR]

The sub-lethal toxicity of Captan® on selected haematological (Hemoglobin, Haematocrit, Mean Corpuscular Hemoglobin) growth (Condition factor, Hepatosomatic Index, Specific Growth Rate), biochemical (serum glucose, protein), and endocrine parameters (growth hormone, T 3 and T 4) in Clarias batrachus was examined under chronic exposures. Captan® was administered at predetermined exposure concentrations (0.53 and 1.06 mg/L) and monitored on days 15, 30, and 45 of the experimental periods. The experimental groups showed significantly lower values (p < 0.05) of haemoglobin content, hematocrit, MCH in Captan® exposed fish compared to control. Serum protein, k-factor and SGR were significantly lower in exposed fish. Endocrine responses (T 3 and T 4) emerged as the most sensitive biomarker category, depicting modulated responses between sub-chronic exposure at day-15 and chronic responses at day-45. In general, biomarker depictions indicate that Captan® exposures are capable of inducing stress-specific effects at the biochemical and physiological levels negatively impacting the overall health and longevity of such animals. [Display omitted] • Captan® chronic effect was tested on biomarkers in Clarias batrachus. • Hematological, growth, endocrine and biochemical biomarkers were examined. • Endocrine responses (T 3 and T 4) emerged as the most sensitive biomarker category. • Thyroid hormones (T 3 and T 4) modulated at day-15 (sub-chronic) and day-45 (chronic). • Sublethal Captan® exposures can impact fish growth and survival in the wild. [ABSTRACT FROM AUTHOR]

Metal exposure impairs respiration, increases metabolic demand, and reduces energy storage/fitness in aquatic species. Respiratory impairment and energy storage was examined in acute selenium-exposed Indian major carps, Catla catla, Labeo rohita and Cirrhinus mrigala fry and were correlated with exposure concentrations. Toxicity effects were determined in a renewal bioassay using 96 h lethal selenium concentrations. Species sensitivity distribution (SSD) was also used to derive predicted no-effect concentrations, toxicity exposure ratios, for selenium exposures to early-life fish stages. Mortality was proportional with increasing concentrations. Oxygen consumption and lipid content compared to moisture and ash and of all protein content in tissues of C. catla and C. mrigala indicates that lowered oxygen consumption is directly predictive of lowered lipid content and selenium-induced hypoxia impacts the energy/nutritional status of the early-life stage of carp. This cross-taxa comparison will have major implications for advancing impact assessment and allow better targeting of species for conservation measures. • Early-life stage survival is critical for population growth and recruitment. • Acute selenium sensitivity in closely related early-stage fish was examined. • Species-specific susceptibility was observed for early-stage fish. • Species-specific toxicity responses were observed. [ABSTRACT FROM AUTHOR]

The widespread occurrence of Mercury (Hg) and its derivatives in the aquatic environment and risks to the health of local populations has necessitated investigations into its toxic effects on sessile species. The toxicity of Mercury was observed sequentially from 96 h acute exposure regime (behavioural endpoints) to chronic durations (haematological and biochemical toxicity endpoints) in Bellamya bengalensis. Time-dependent lethal endpoints for acute toxicity (LC50) of mercury i.e., 24,48,72 and 96 h were estimated as 0.94, 0.88, 0.69 and 0.40 mg/l respectively. Threshold effect values i.e., LOEC (Lowest Observed Effect Concentration), NOEC (No Observed Effect Concentration) and MATC (Maximum Acceptable Toxicant Concentration) at 96 h were found to be 0.10, 0.05, 0.039 mg/l respectively. The study of oxygen consumption rate and behavioural changes during acute toxicity and haematological and biochemical responses during chronic toxicity to sublethal concentrations (10% and 20% of 96 h LC50) of mercury to the snail were also conducted. The organisms showed initial elevation at 24 h but later gradual decrease in oxygen consumption rate with the increase of concentration of mercury and time of exposure. For behavioural studies, variable test concentrations from 0.00 to 1.00 mg/l were used for 24, 48, 72 and 96 h. The crawling activity and clumping tendency decreased with the progress of time at all treatment periods and stopped ultimately at 96 h of exposure from 0.7 mg/l onwards whereas touch reflex was not observed at 96 h exposure at all treatments except at 0.09 mg/l. In haemocyte count, no significant variation was observed among control values between various exposure periods (p > 0.05) though variations were observed in sub-lethal concentrations versus control at all treatment duration (7, 14, 21, 28d, p < 0.05). In biochemical response study, the protein content in hepatopancreas of the snails treated at sublethal concentrations of mercury (10% and 20% of 96 h LC50) reduced significantly versus control after 21d of exposure (p < 0.05). In gonads, the protein content of the treated snails significantly reduced at all treatment concentrations versus control at all exposure times (p < 0.05). Based on the safe levels indicated above, the concentration of 0.01 to 0.04 ppm of mercury can be considered safe for Bellamya bengalensis and any less-hardy aquatic species. These responses elicited by our molluscan model will not only help in biomonitoring of environmental mercury contamination in water bodies but will also provide support to ecological health and risk assessment. [Display omitted] • Toxic responses of mercuric chloride (HgCl 2) to freshwater snail, Bellamya bengalensis was determined • Mortality of the snails increased with elevated mercury concentrations and increase duration of exposure. • Altered behavioral responses and decreased oxygen consumption were concentration-dependent • Reduced protein levels in hepatopancreas portend risks of impaired protein synthesis [ABSTRACT FROM AUTHOR]

There is limited information on fluoride toxicity and risk overview on ecotoxicological risks to aquatic invertebrate populations particularly molluscan taxa. This necessitated the assessment of toxicity responses in the freshwater snail, Bellamya bengalensis exposed to environmentally relevant concentrations of sodium fluoride. Under lethal exposures (150, 200, 250, 300, 400 and 450 mg/l), the median lethal concentrations (LC 50) were determined to be 422.36, 347.10, 333.33 and 273.24 mg/l for B. bengalensis at 24, 48, 72 and 96 h respectively. The rate of mortality of the snails was increased significantly with elevated concentrations of the toxicant. The magnitude of toxicity i.e., toxicity factor at different time scale was also higher with increased exposure duration. Altered behavioural changes i.e., crawling movement, tentacle movement, clumping tendency, touch reflex and mucous secretion in exposed snail with elevated concentrations and exposure duration. Similarly, oxygen consumption rate of the treated snail also lowered significantly during 72 and 96 h of exposure. Under 30-day chronic exposures (Control-0.00 mg/L; T1–27.324 mg/L; T2–54.648 mg/L) , protein concentrations in gonad and hepatopancreas of exposure groups was significantly lowered. Chronic exposures also revealed lowered haemocytes counts in exposure groups. The potential for loss of coordination, respiratory distress and physiological disruption in organisms exposed to environmentally relevant concentrations of fluoride was demonstrated by this study. The estimation and magnitude of toxicity responses are necessary for a more accurate estimation of ecological risks to molluscan taxa and invertebrate populations under acute and chronic fluoride exposures in the wild. [Display omitted] • Responses in NaF-exposed freshwater snail, Bellamya bengalensis was estimated. • Mortality increased with elevated fluoride concentrations and increasing exposure period. • Altered behavior and lowered oxygen consumption were concentration-dependent. • Decreased haemocyte count could impact respiratory capacity. • Reduced protein content in hepatopancreas indicate impaired protein synthesis. [ABSTRACT FROM AUTHOR]

The present study was aimed to evaluate the toxic effects of a commonly used synthetic pyrethroid, λ cyhalothrin on the common carp, Cyprinus carpio L. The results depicted that 96 h LC 50 value of λ cyhalothrin to the fish was 1.48 μg l−1. During 45 days of chronic exposure a significant reduction (p < 0.05) in the RBC, hemoglobin, and hematocrit value of fish was observed in λ cyhalothrin treated fish. Blood glucose, cholesterol and creatinine levels increased significantly, while total protein and albumin were significantly decreased (p < 0.05) in the exposed fish. Moreover, alanine aminotransferase and aspartate aminotransferase levels in the blood also increased significantly (p < 0.05) in the treated fish. In gills and liver, glutathione S-transferase (GST) and glutathione peroxidase (GPx) and in liver GST exhibited a significant initial augmentation followed by a subsequent reduction while catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA) level increased markedly with incrementing concentrations of λ cyhalothrin in both the organs. Acetylcholinesterase (AchE) activity in both gills and liver decreased in exposed fish upon addition λ cyhalothrin. However, the hazardous effects of λ cyhalothrin on C. carpio were characterized and portrayed by the development of integrated biomarker response (IBR), and biomarker response index (BRI). GUTS-SD and IT modeling were implied for a better interpretation of the toxicity. These results indicate that exposure to λ cyhalothrin alters the survivability at the acute level and the activity of hematological, plasma biochemical as well as enzymological and stress parameters (in gills and liver) at the sublethal level in C. carpio. [Display omitted] • λ cyhalothrin acutely altered survivability and behavior in Cyprinus carpio L. • λ cyhalothrin sublethally altered hematological and plasma biochemical parameters in Cyprinus carpio L. • λ cyhalothrin imparts negative effect on stress enzyme parameters in gills and liver of Cyprinus carpio L. • T2-30d is the most affected group of fish according to the IBR index. • BRI portrays that λ cyhalothrin causes major alterations on exposed Cyprinus carpio L. [ABSTRACT FROM AUTHOR]

[Display omitted] • Alpha-cypermethrin altered survivability and behavior in Cyprinus carpio L. • A-cyp altered haematological parameters in C. carpio L. during sublethal exposure. • A-cyp altered biochemical parameters in C. carpio L. during sublethal exposure. • T2-45d is the most affected fish group according to IBR index. • BRI portrays that A-cyp causes moderately adverse effects on C. carpio L. This study assessed some important physiological biomarkers of freshwater edible fish Cyprinus carpio following exposure to 10 % (T1) and 20 % (T2) sublethal concentrations of Alpha-cypermethrin (A-cyp) over a total period of 45 days. Behavioral responses were noticed and Kaplan-Meier survival curves were prepared during acute toxicity study. Total serum protein concentration, total erythrocyte count, hemoglobin, packed cell volume, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, and total leukocytes count were decreased significantly (p < 0.05), while the blood glucose, total serum lipid concentration, and clotting time were increased significantly (p < 0.05) over control. The most affected fish group and most significantly altered biomarker under toxic stress of A-cyp were identified using integrated biomarker response (IBR). The biomarker response index (BRI) values measured the overall health status of the treated fish and indicated that moderate adverse effects were exerted on the fish group exposed to T2 for 45 days. [ABSTRACT FROM AUTHOR]

The present study was performed to determine the acute toxicity of sodium laureth sulfate (SLES) and its sublethal effects on oxidative stress enzymes in benthic oligochaete worm Tubifex tubifex. The results showed that 96 h median lethal concentration (LC 50) value of SLES for Tubifex tubifex is 21.68 mg/l. Moreover exposed worms showed abnormal behaviours including incremented erratic movement, mucus secretion, and decreased clumping tendency at acute level. Percentage of autotomy additionally increased significantly (P < 0.05) with the increasing dose of toxicant at 96 h exposure. Sublethal concentrations of SLES (10% and 30% of 96 h LC 50 value) caused paramount alterations in the oxidative stress enzymes. Superoxide dismutase (SOD), reduced glutathione (GSH), glutathione S-transferase (GST), and glutathione peroxidase (GPx) exhibited a striking initiatory increment followed by a resulting descending pattern. Moreover, during exposure times, catalase (CAT) activity and malondialdehyde (MDA) level increased markedly with incrementing concentrations of SLES. However, the effects of sodium laureth sulfate on Tubifex tubifex were characterized and portrayed by the development of a correlation matrix and an integrated biomarker response (IBR) assessment. These results indicate that exposure to this anionic surfactant alters the survivability and behavioral response at acute level and modifies changes in oxidative stress enzymes at sublethal level in Tubifex tubifex. Unlabelled Image • The toxic effects of sodium laureth sulfate (SLES) were investigated in Tubifex tubifex. • SLES exposure induced mortality, autotomy, and changes in behavioral responses in Tubifex tubifex at an acute level. • SLES exposure altered the levels of oxidative stress biomarkers in Tubifex tubifex. [ABSTRACT FROM AUTHOR]

The present study was aimed to assess the acute toxicity of organophosphate pesticide, profenofos; synthetic pyrethroid pesticide, λ cyhalothrin and biopesticide, azadirachtin and their sublethal effects on growth rate and oxidative stress biomarkers in Tubifex tubifex in vivo. The results showed that 96 h LC 50 value of profenofos, λ cyhalothrin and azadirachtin to Tubifex tubifex are 0.59, 0.13 and 82.15 mg L−1 respectively. Pesticide treated worms showed several behavioral abnormalities including increased mucus secretion, erratic movements, wrinkling activity and decreased clumping tendency during acute exposure. The percentage of autotomy increased significantly (p < 0.05) with the increasing concentration of the pesticides at 96 h of exposure. Sublethal concentrations of profenofos (0.059 and 0.118 mg L−1), λ cyhalothrin (0.013 and 0.026 mg L−1) and azadirachtin (8.2 and 16.4 mg L−1) caused significant alterations in growth rate and oxidative stress enzymes in T. tubifex during 14 days exposure period. The growth rate of the pesticide exposed worms decreased significantly (P < 0.05) in a concentration and duration-dependent manner. Superoxide dismutase (SOD), reduced glutathione (GSH), glutathione-s-transferase (GST) and glutathione peroxidase (GPx) demonstrated a noteworthy (p < 0.05) initial induction followed by a subsequent reduction, while catalase (CAT) and malondialdehyde (MDA) exhibited noteworthy induction (p < 0.05) all through the exposure time. Through principal component analysis, correlation matrix, and integrated biomarker response, the effects of profenofos, λ cyhalothrin and azadirachtin on T. tubifex were distinguished. These results indicate that exposure to profenofos, λ cyhalothrin and azadirachtin affect survivability, change the behavioral responses, reduce the growth rate and induce oxidative stress enzymes in T. tubifex. Unlabelled Image • The potential toxic effects of pesticide profenofos, λ cyhalothrin and biopesticide, azadirachtin were investigated in worm, Tubifex tubifex. • Exposure to profenofos, λ cyhalothrin and azadirachtin altered the behavioral responses, growth rate and activities of oxidative stress biomarkers in T. tubifex. • Indiscriminate use of these pesticides for agricultural and household purposes could serve as a potential threat to aquatic organisms. [ABSTRACT FROM AUTHOR]

The present study was assessed to determine the in vivo toxic effects of a cationic surfactant, cetylpyridinium chloride (CPC), and an anionic surfactant, sodium dodecyl sulfate (SDS) in terms of oxidative stress biomarkers in benthic oligochaete worm Tubifex tubifex for 14 days. The investigation demonstrated that sublethal concentrations of CPC (0.0213, and 0.0639 mg L−1) and SDS (1.094 and 3.092 mg L−1)induced paramount alterations in the oxidative stress enzymes in Tubifex tubifex. Superoxide dismutase (SOD), glutathione S-transferase (GST), reduced glutathione (GSH), and glutathione peroxidase (GPx) exhibited an initial notable increase in their activities in the surfactants exposed worms at 1d and 7d of exposure period followed by consequential reduction at 14d exposure period with respect to control, while catalase (CAT) and malondialdehyde (MDA) activities markedly incremented gradually throughout the exposure periods. Through the construction of the correlation matrix and integrated biomarker response (IBR), the effects of CPC and SDS on Tubifex tubifex were distinguished. These results indicate that exposure to these cationic and anionic surfactants modulates the levels of oxidative stress enzymes in Tubifex tubifex. Unlabelled Image • The potential toxic effects of a cationic surfactant, cetylpyridinium chloride (CPC), and an anionic surfactant, sodium dodecyl sulfate (SDS) were investigated in benthic oligochaete worm, Tubifex tubifex. • Exposure to CPC and SDS altered the activities of oxidative stress biomarkers in Tubifex tubifex. • Incongruous disposal of these surfactants in water bodies could serve as a potential threat to aquatic health. [ABSTRACT FROM AUTHOR]