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Significant DNA damage was observed in hemolymph of molluscs exposed to raw composite tannery effluent as evident from comet assay images. DNA damage was evaluated by the presence of tail resembling that of comet in single strand DNA. Break in DNA strand was reported in the liver and gill Iodophenpropit dihydrobromide of catfish in response to dye containing textile industrial effluent (Banerjee et al., 2014). The figure indicates that no DNA damage was observed in molluscs hemolymph in control, as well as, in both the MF treated and MF+RO treated effluents (p<0.005). Comet assay in the hemolymph of Mytilus galloprovincialis reflected low level of DNA damage in lower level of genotoxic contaminants whereas in summer, increased anthropogenic activity resulted in higher level of DNA damage suggesting that comet assay can be evaluated as sensitive biomarker for detection of lower level of toxicant exposure of marine organism (Almeida et al., 2013). Therefore the present observations suggest that the membrane based treatments enable to reduce the toxicity of the composite tannery effluent to considerable extent, thereby eliminating the DNA damages. Histocytopathological studies in selected tissues of bivalves are widely used as biomarker for biomonitoring marine pollution. This study reveals the status of target tissues in response to pollution and provides a general view of damage as observed from tissue damage received by molluscs (Carballeira et al., 2011). The results suggested that a two-stage membrane filtration (MF+RO) of untreated effluent reduced the stress causing factors which were evident from the histological studies of the mantle and gonad.
Conclusions Toxic impacts of a composite effluent from tannery industry were evaluated using snail, P. globosa as an aquatic model. The effect of a single stage MF treatment and a two-stage treatment involving MF+RO was observed on the aquatic life to assess the efficiency of the membrane based processes with respect to toxicity reduction in the environment. P. globosa was found to respond severely in the untreated effluent with significant increase in the SOD and CAT activity, viz. about ∼1.5 folds ∼2.9 folds, respectively in the body tissue. In addition, the protein content also reduced to about 37% after 96h of exposure of P. globosa to untreated effluent. On the other hand, the MF treated and MF+RO treated effluent did not show significant effect (p<0.05) on Pila. The protein, amino acid and carbohydrate content for the treated effluents were comparable to that of the control. DNA damage in the hemolymph of molluscs exposed to the untreated effluent was evident from comet assay, while in membrane treated effluents showed no significant DNA damage. After 96h of exposure to the untreated effluent, about 80% mortality for Pila sp. was observed while 11% mortality for the MF treated and no mortality for MF+RO treated effluent was observed. Histopathological study revealed damages in the epithelial layers and muscle bands of both mantle and gonad tissues for the untreated effluent and less damage for MF treated effluent while no damage for MF+RO treated effluent.
Introduction Increasing cases of multidrug-resistant strains of Acinetobacter baumannii, Pseudomonas aeruginosa and Klebsiella pneumoniae [1,2] has led to the reintroduction of the last resort antibiotic, colistin, into clinical practice [3,4]. Colistin (polymyxin E) is a cationic polypeptide with bactericidal activity against multidrug resistant gram-negative pathogens [5,6]. Nephrotoxicity and neurotoxicity of colistin after intramuscular or intravenous administration of patients have been reported [7,8]. Although, the current dosage regimens are not likely to predispose patients to neurotoxicity compared to nephrotoxicity [7], there are increasing cases of neurotoxicity [9,10]. Neurotoxicity of colistin is linked to its ability to penetrate blood brain barrier, blood-cerebrospinal fluid and accumulate in the brain [[10], [11], [12]]. Although, colistin does not disrupt blood brain barrier, it transverses the barrier through the organic cation transporters 1 and 2 [10]. In addition, the peptide like features of colistin facilitate its uptake into the brain through parenchyma polypeptide transporter [13,14]. Associated neurological symptoms of colistin include confusion, dizziness, facial and peripheral paraesthesia, visual disturbances, muscle weakness, hallucination, vertigo, seizures and ataxia [5,15]. This is consistent with animal studies that demonstrated marked neurobehavioural changes, including muscular weakness and ataxia, in mice or rats [[16], [17], [18]].