Response of gill ATPase and liver esterase of pseudorasobora parva to a two month exposure to glyphosate and metsulfuron methyl

Responses of gill ATPase and liver esterase of topmouth gudgeon, Pseudorasobora parva under sublethal exposure to glyphosate (WSC 41% as isopropyl amine salt) at 1.0, 5.0 and 25?mg/L and metsulfuron methyl (technical 98.2%) at 0.0095, 0.085 and 0.85?mg/L of water were measured at 8th, 16th, 24th and 65th days of exposure. Two way analysis of variance (ANOVA) followed by least significant difference (LSD) test and parameter estimates indicated a significant inhibitory effect on gill ATPase activity (max. 57%) by metsulfuron methyl and liver esterase activity by glyphosate (max. 43%) as compared to the control, but the differences in the residual activities among the concentration levels of the herbicides were not significant. The activities changed significantly with the sampling times except gill ATPase activity under metsulfuron methyl exposure. In most of the cases, the maximum inhibitory effect on the enzymes was recorded on the 8th day and over-recovering appeared with time.     

The mechanism of delayed neuropathy caused by some organophosphorus esters: Using the understanding to improve safety

Abstract

The mechanism of delayed neurotoxicity of some OP (organophosphorus) esters such as DFP (di‐isopropyl phosphorofluoridate) and TOCP (tri‐o‐cresyl phosphate) involves an initial two‐step process affecting an esterase called NTE (neurotoxic esterase). This understanding permits the assessment of delayed neuropathic potential in terms of a quantitative measurement of inhibition of NTE in tissue taken from dosed hens. Structure/activity relationships have been rationalized and the neurotoxic potential of those OP esters which are direct inhibitors of esterases may now be assessed in vitro. The response of human NTE can usefully be compared with that of hen NTE. Nil delayed neurotoxic potential is associated with carbamate or phosphinate anticholinesterases which may be designed as insecticides.     

Assessment of risks, implications, and opportunities of waterborne neurotoxic pesticides

Pesticides are a well-known family of chemicals that have contaminated water systems globally. Four common subfamilies of pesticides include organochlorines, organophosphates, pyrethroids, and carbamate insecticides which have been shown to adversely affect the human nervous system. Studies have shown a link between pesticide exposure and decreased viability, proliferation, migration, and differentiation of murine neural stem cells. Besides human exposure directly through water systems, additional factors such as pesticide bioaccumulation, biomagnification and potential synergism due to co-exposure to other environmental contaminants must be considered. A possible avenue to investigate the molecular mechanisms and biomolecules impacted by the various classes of pesticides includes the field of -omics. Discovery of the precise molecular mechanisms behind pesticide-mediated neurodegenerative disorders may facilitate development of targeted therapeutics. Likewise, discovery of pesticide biodegradation pathways may enable novel approaches for water system bioremediation using genetically engineered microorganisms. In this mini-review, we discuss recently established harmful impacts of various categories of pesticides on the nervous system and the application of -omics field for discovery, validation, and mitigation of pesticide neurotoxicity.     

Inhibitory Effects on Esterase Enzymes Buche and Ache in Rainbow Trout (Oncorhyncus mykiss) Produced by the Slow Release Insecticide Chitosan Diethyl Phosphate

The study on the toxicity of chitosan diethyl phosphate (ChDP), a controlled release insecticide, on the activities of butyrylcholinesterase (BuChE) and acetylcholinesterase (AChE) in rainbow trout exposed to this pesticide was carried out. It was found that ChDP reduced BuChE activity in O. mykiss by a factor of eight at 6 days, with high fluctuation to the end of the exposition time at 12 days. The in vitro analysis of brain AChE treated with ChDP and Phenamiphos showed that it was competitively inhibited by both organophosphates. The values obtained for K_m and V_max for the AChE-ChDP (K_m: 21.23 μ M; V_max: 43.10 μ mol/min/g) and AChE-Phenamiphos (K_m: 38.62 μ M; V_max: 38.91 μ mol/min/g) systems were relatively low compared to values of the AChE (control) system (K_m: 62.99 μ M; V_max: 63.29 μ mol/min/g). Results reported in this study confirmed that chitosan diethyl phosphate performs similarly to organophosphate pesticides, producing inhibition in cholinesterases in rainbow trout.     

Subcellular distribution op neurotoxic esterase activity in lamb and mouse brain

Abstract

Brain tissue samples of nice (7.5 g from 25 mouse brains and lamb (25 g) were homogenized and subcellular fractions prepared in order to assay the distribution of neurotoxic esterase (NTE) activity. The specific inhibitor, N,N‐diisopropylphosphorodiamidic fluoride (mipafox) was synthesized and purified. Maximum specific activity of NTE was reached in the microsomal fraction (110,000 g) while the enzyme activity in the soluble fraction (110,000 g) was extremely low. This subcellular distribution of NTE activity in mammal brains is an original contribution. Brain microsomal fraction is suggested to be a more reliable source for the highest activity of NTE. The specific activity of NTE of lamb brain was much higher than that of mouse brain. This night help interpretation of the characteristic species variation in susceptibility to NTE inhibitors which are known to be potent delayed neurotoxic agents.     

Copper and cadmium effects on growth and extracellular exudation of the marine toxic dinoflagellate Alexandrium catenella: 3D-fluorescence spectroscopy approach

In this study, metal contamination experiments were conducted to investigate the effects of copper and cadmium on the growth of the marine toxic dinoflagellate Alexandrium catenella and on the production of dissolved organic matter (Dissolved Organic Carbon: DOC; Fluorescent Dissolved Organic Matter: FDOM). This species was exposed to increasing concentrations of Cu²⁺ (9.93 × 10⁻¹⁰–1.00 × 10⁻⁷ M) or Cd²⁺ (1.30 × 10⁻⁸–4.38 × 10⁻⁷ M), to simulate polluted environments. The drastic effects were observed at pCu²⁺ = 7.96 (Cu²⁺: 1.08 × 10⁻⁸ M) and pCd²⁺ = 7.28 (Cd²⁺: 5.19 × 10⁻⁸ M), where cyst formation occurred. Lower levels of Cu²⁺ (pCu²⁺ > 9.00) and Cd²⁺ (pCd²⁺ > 7.28) had no effect on growth. However, when levels of Cu²⁺ and Cd²⁺ were beyond 10⁻⁷ M, the growth was totally inhibited. The DOC released per cell (DOC/Cell) was different depending on the exposure time and the metal contamination, with higher DOC/Cell values in response to Cu²⁺ and Cd²⁺, comparatively to the control. Samples were also analyzed by 3D-fluorescence spectroscopy, using the Parallel Factor Analysis (PARAFAC) algorithm to characterize the FDOM. The PARAFAC analytical treatment revealed four components (C1, C2, C3 and C4) that could be associated with two contributions: one, related to the biological activity; the other, linked to the decomposition of organic matter. The C1 component combined a tryptophan peak and a characteristic humic substances response, and the C2 component was considered as a tryptophan protein fluorophore. The C3 and C4 components were associated to marine organic matter production.     

Chlorination-induced cellular damage and recovery in marine microalga, Chlorella salina

Power plants employ chlorination for controlling biofouling in the cooling water system. Phytoplankton drawn into the cooling water system could be impacted by chemical stress induced by the oxidizing biocide. It is likely that microalgae, being sensitive to chlorine, could suffer damage to their cellular structure and function. In this study, we present data on the effect of in-use concentrations of chlorine on the unicellular microalga, Chlorella salina. Chlorophyll autofluorescence was measured in terms of mean fluorescence intensity per cell for rapid assessment of toxicity. Viability of the cells exposed to chlorine was determined by fluorescein diacetate staining. Functionality of the photosynthetic machinery was assessed by gross primary productivity. Results from the study, which combined confocal laser scanning microscopy with image analysis, showed a significant dose-dependant reduction in chlorophyll autofluorescence, esterase activity and gross primary productivity in chlorine-treated cells. Interestingly, the cells injured by chlorination could not recover in terms of autofluorescence, esterase activity or productivity even after 18 h incubation in healthy media. Among the test points evaluated, esterase activity appeared to be sensitive for determining the chlorination-induced impact. Our results demonstrate that low-dose chlorination causes significant decrease in chlorophyll autofluorescence, intracellular esterase activity and primary productivity in Chlorella cells.