Clinicohematological, Mutagenic, and Oxidative Stress Induced by Pendimethalin in Freshwater Fish Bighead Carp (Hypophthalmichthys nobilis)

Abstract

Currently, aquatic and terrestrial ecosystems are continuously and chronically polluted by cocktails of countless chemical compounds. The susceptibility to infections is tremendously increasing in a variety of organisms due to exposure to environmental pollutants. Pendimethalin, an herbicide, is continuously used in agriculture to remove unwanted broadleaf weeds across the globe. Therefore, this study investigates the mechanisms of toxicity of pendimethalin in freshwater fish bighead carp upon exposure to low and environmentally relevant concentrations. For this purpose, 48 fish without any clinical abnormalities were kept in a glass aquarium in different experimental groups (T0, T1, T2, and T3). These groups were treated with pendimethalin at 0.00, 0.25, 0.50, and 0.75 mg/L, respectively. Four fish were randomly picked from each experimental group and killed at 72, 96, and 120 hours of the trial to study hematobiochemical parameters and visceral tissues including the brain, liver, heart, gills, and kidneys for histopathology. Herbicide-treated fish indicated various physical and behavioral abnormalities including hypersecretion of mucus, erratic swimming, operculum movement, air gulping, tremors of fins, loss of equilibrium, and increased surface breathing. Histopathologically, gills tissues of treated fish indicated atrophied lamellae, uplifting of secondary lamellae, necrosis of primary and secondary lamellar epithelial cells, telogenesis, congestion, and lamellar fusion. Histopathological examination of liver tissues of treated fish showed mild to moderate congestion, necrosis of hepatocytes, and atrophy of hepatocytes while kidneys revealed degeneration of renal tubules, glomerular atrophy, ceroid, and necrosis of renal tubules. The erythrocyte counts, monocyte and lymphocyte counts, and hemoglobin values were significantly ( P < 0.05 ) reduced in pendimethalin-treated fish. Results on serum biochemistry showed that the biomarkers of kidneys, heart, and liver were significantly higher in fish of treated groups. In addition, values of different biochemical reactions like reactive oxygen species (ROS), thiobarbituric acid reactive species (TBARS), total proteins, and quantity of different antioxidant enzymes including reduced glutathione (GSH), catalase, and superoxide dismutase (SOD) were significantly different when compared to untreated fish. Moreover, the percentile of different nuclear abnormalities in red blood cells and frequency of DNA damage increased significantly in treated fish. It can be concluded from the findings that pendimethalin causes its toxic effects via disruption of physiological and hematobiochemical reactions of fish.

[Retracted] Acetochlor Affects Bighead Carp (Aristichthys Nobilis) by Producing Oxidative Stress, Lowering Tissue Proteins, and Inducing Genotoxicity

“…Significantly ( P ≤ 0.05) increased oxidative stress parameters were observed in the liver and the brain of fish treated with acetochlor, in the present study. Increased oxidative stress in the brain may be the effect of the induction of neurotransmitters and stress hormones released in the brain due to acetochlor treatment [ 65 , 66 ]. In the current study, total protein and GSH contents in various tissues of bighead carp could be attributed to reduced tissue activities, higher usage of energy/body proteins to counteract oxidative stress, and lower protein levels in the body and tissues.…”

Evaluation of DNA Damage, Biomarkers of Oxidative Stress, and Status of Antioxidant Enzymes in Freshwater Fish (Labeo rohita) Exposed to Pyriproxyfen

“…However, other than fish species, DNA damage was also observed in other organisms like birds and mammals [72], rats [6], chickens [73], liver cancer cell line [74,75], and HepG2 cell line [76]. In contrast to the results on comet assay, no significant increase in DNA damage due to toxicant has been observed in fish [77][78][79]. Moreover, it can be speculated that DNA damage in different tissues of Labeo rohita might also be related to genetic abnormalities induced by PPF leading to the activation of abnormal and physiologically nonfunctional proteins responsible for mitochondrion dysfunctioning and breakage of nuclear proteins [80,81].…”

Evaluation of Hematological, Oxidative Stress, and Antioxidant Profile in Cattle Infected with Brucellosis in Southern Punjab, Pakistan

“…Oxidative stress performs a vital role in the development of clinical disease and also leads to DNA damage, enzymic deactivation, lipid peroxidation, apoptosis, and cell necrosis [64][65][66][67][68][69][70]. With the declining body's antioxidantbased defense mechanism, oxidative stress concentration gets enhanced in brucellosis [71][72][73].…”