In vivo assessment of dichlorvos induced histological and biochemical impairments coupled with expression of p53 responsive apoptotic genes in the liver and kidney of fish, Channa punctatus (Bloch, 1793).

Sub-lethal exposure of dichlorvos induces oxidative stress, consequent genetic instability and apoptosis coupled with impairments in biochemical, histopathological and transcription of genes in Channa punctatus. Exposure of 5% (0.041 mg/L; E2) and 10% (0.082 mg/L; E3) of 96 h-LC50 of dichlorvos significantly (p < 0.05) elevated the reactive oxygen species (ROS) generation and activities of SOD and CAT, as compared to control (E1) after 30 d. The maximum reduction in reduced glutathione (GSH) was recorded in the liver (18.53 ± 0.81 µg/mg of protein) and kidney (19.32 ± 0.97 µg/mg of protein); while the total protein contents were also found reduced, 278.38 ± 8.40 µg/mL (liver) and 248.44 ± 7.28 µg/mL (kidney), after 30 days in E3, in comparison to respective controls. Further, significant (p < 0.05) induction in micronuclei (MN) and apoptotic cells (AC), in a dose- and exposure-based manner were also recorded. Moreover, a significant (p < 0.05) up-regulation of p53 (2.51-fold in liver), bax (2.03-fold in liver; 1.99-fold in kidney) and casp3a (2.26-fold in liver; 2.10-fold in kidney) together with an elevated expression of cat (1.73-fold in liver; 1.12-fold in kidney), p53 (1.27-fold in kidney) and apaf-1 (1.72-fold in liver) in fish exposed to higher dose of dichlorvos for 30 d evidently reflects geno-toxicological potential of referenced pesticide. Disturbed biochemical and molecular parameters evince that the fish experienced oxidative stress as is further supported by prominent pathological observations in liver and kidney. Findings are, thus, helpful in organ-specific molecular scanning against aquatic toxicants like dichlorvos.

Biomonitoring of Heavy Metals in River Ganga Water, Sediments, Plant, and Fishes of Different Trophic Levels.

In this study, the pattern of metals concentration in water, sediment, plants, and three edible fish species (Channa striata, Labeo rohita, and Catla catla) of different trophic levels, captured from Jajmau (Kanpur), an important fishery area of river Ganga in Uttar Pradesh, India was examined. The heavy metals, Ni, Pb, Fe, Cu, Zn, Cd, Cr, and Co, were estimated in the liver, kidney, muscles, and gill tissues of abovesaid species of fish. The highest metal concentration was reported in the bottom feeder fish as compared with the column and surface feeders. The result obtained after analysis of water sample reflects the order of occurrence of heavy metals as Fe > Cr > Pb > Ni > Cd > Zn > Cu > Co. Sediments analysis indicates high concentration of Fe and Cr, making the entire environment from top to bottom, stressful. Target hazard quotient (THQ) and hazard index (HI) of the three species suggest a potential risk to the health of consumers, the humans. Thus, it is inevitable that the river Ganga should be closely monitored to safeguard human health. Graphical Abstract.

A protective study of curcumin associated with Cr6+ induced oxidative stress, genetic damage, transcription of genes related to apoptosis and histopathology of fish, Channa punctatus (Bloch, 1793).

Ameliorative potential of curcumin against Cr6+-induced eco-toxicological manifestations was assessed in liver of exposed Channa punctatus (Actinopterygii) in six groups for 45 d; Group I as control. Group II with 3 mg/L of curcumin; group III with 7.89 mg/L of Cr6+. Groups IV, V and VI were simultaneously co-exposed with 7.89 mg/L of Cr6+ and three different curcumin concentrations, 1, 2, and 3 mg/L, respectively. In group III, SOD-CAT, GR significantly (p < 0.05) increased; decreased GSH level; elevated MN and AC frequencies; and a significant (p < 0.05) up-regulation of cat (2.72-fold), p53 (1.73-fold), bax (1.33-fold) and apaf-1 (2.13-fold) together with a significant (p < 0.05) down-regulation of bcl-2 (0.51-fold). Co-exposure significantly (p < 0.05) brought down activities of SOD-CAT, GR, raised GSH, decreased micronuclei and apoptotic frequencies along with recovery of histopathological anomalies in liver. This study establishes the protective role of curcumin against Cr6+-induced hepatotoxicity in fish.

An in vivo analysis of Cr6+ induced biochemical, genotoxicological and transcriptional profiling of genes related to oxidative stress, DNA damage and apoptosis in liver of fish, Channa punctatus (Bloch, 1793).

Present study was designed to assess the hexavalent chromium (Cr6+) mediated oxidative stress that induces DNA damage and apoptosis in adult fish, Channa punctatus (35 ±â€¯3.0 g; 14.5 ±â€¯1.0 cm; Actinopterygii). Fishes were maintained in three groups for 15, 30 and 45 d of exposure periods. They were treated with 5% (Group T1) and 10% (Group T2) of 96 h-LC50 of chromium trioxide (Cr6+). Controls were run for the similar duration. A significant (p < 0.05) increment in the activities of antioxidant enzymes, SOD and CAT in liver tissues of the exposed fish evinces the persistence of oxidative stress. A significant (p < 0.05) increase in induction of micronuclei (MN) coupled with transcriptional responses of target genes related to antioxidant enzymes, DNA damage and apoptosis (sod, cat, gsr, nox-1, p53, bax, bcl-2, apaf-1 and casp3a) establishes the impact of oxidative stress due to in vivo, Cr6+ accumulation in liver as compared to control (0 mg/L), in a dose and exposure-dependent manner. Initially, the increased level of reactive oxygen species (ROS) in liver coincided with that of enhanced mRNA expression of antioxidant enzymes, sod, cat, gsr and nox-1 but, later, the overproduction of ROS, after 45 d of exposure of Cr6+, resulted in a significant (p < 0.05) up-regulation of p53. Our findings also unveil that the up-regulation of bax, apaf-1 and casp3a and down-regulation of bcl-2 are associated with Cr6+-induced oxidative stress mediated-apoptosis in liver of test fish. Aforesaid molecular markers can, thus, be efficiently utilized for bio-monitoring of aquatic regimes and conservation of fish biodiversity.

Zn2+ induced molecular responses associated with oxidative stress, DNA damage and histopathological lesions in liver and kidney of the fish, Channa punctatus (Bloch, 1793).

Zn2+ is essential for normal physiological functioning of all organisms in small quantities, but when its concentration enhances in surrounding environment it acts as a toxicant to organisms. Common sources of Zn2+ pollution are electroplating, alloying, mining, and allied industrial operations. The present study aims to assess the biochemical, histopathological and genotoxicological implications under Zn2+ intoxication along with its accumulation patterns in prime biotransformation sites-liver and kidney, of a bottom feeder fish, Channa punctatus. Fish were chronically exposed to two different concentrations of Zn2+i.e., 5mg/L (permissible limit, T1) and 10mg/L (twice the permissible limit, T2). Simultaneous control was maintained. A significant (p<0.05) increment in Zn2+ bioaccumulation, antioxidant enzymes activities of SOD, CAT and GR and induction in micronuclei frequencies along with the significant (p<0.05) decrement in total protein and GSH were observed in all the exposed groups after 28 d. Altered biochemical parameters coupled with enhanced induction in micronuclei and accumulation of Zn2+ in liver and kidney of fish can be regarded as sensitive biomarkers of Zn2+ induced toxicological manifestations and thus, they may be effectively utilized for reliable ecotoxicological biomonitoring of aquatic regimes polluted with Zn2+.

Phorate induced oxidative stress, DNA damage and differential expression of p53, apaf-1 and cat genes in fish, Channa punctatus (Bloch, 1793).

The present study was conducted to assess the in-vivo activities of certain molecular biomarkers under the impact of phorate exposure. Fish, Channa punctatus (35 ± 3.0 g; 14.5 ± 1.0 cm; Actinopterygii) were subjected to semi-static conditions having 5% (0.0375 mg/L for T1 group) and 10% of 96 h-LC50 (0.075 mg/L for T2 group) of phorate exposure for 15 and 30 d. The oxidative stress was assessed in terms of superoxide dismutase (SOD) and catalase (CAT) activities. DNA damage was measured as induction of micronuclei (MN) and consequent differential expression of apoptotic genes-tumor suppressor (p53), apoptotic peptidase activating factor-1 (apaf-1) and catalase (cat) in liver and kidney, two major sites of biotransformation in fish, were quantified. Our findings reveal significant (p < 0.001) augmentations in SOD and CAT activities of liver and kidney tissues. MN frequency in erythrocytes of fish also increases significantly (p < 0.05) in a dose- and time-dependent manner. The mRNA level of p53 increased significantly (p < 0.05) in liver at 10% of 96 h-LC50 of phorate exposure after 30 d suggesting generation of stress due to accumulation of reactive oxygen species (ROS). Eventually, these findings decipher the dual role of ROS in generating genotoxicity as is evident by micronuclei induction and differential regulation of p53, apaf-1 and cat genes during the phorate induced DNA damage and apoptosis in test fish. The experimental inferences drawn on the basis of activities of aforesaid biomarkers shall be helpful in elucidating the possible causes of apoptosis under stressful conditions. Further, this study finds ample application in biomonitoring of phorate polluted aquatic ecosystem.