Abstract:This study was aimed at assessing the histopathological and haematological effects of a widely used herbicide on rice paddy fields, i.e. butachlor, on rainbow trout. Fish were exposed to butachlor at a concentration of 0.39 mg/l, for a period of 10 days. Haematologically, fish showed a significant decrease in erythrocyte count, haemoglobin, white blood cells and lymphocytes and a significant increase in neutrophils compared to controls (P < 0.05). Histopathological observations of prepared sections of the trea… Show more
“…Group III animals administered with lead acetate @265ppm exhibited mild congestion with tubular degeneration (Plate 9). Kidney section of rats of group IV co-administered with butachlor @262mg/kg and lead acetate @265ppm showed moderate degeneration of epithelial cells of PCT, hypercellularity of glomeruli, and presence of intra tubular hyaline cast (Plate 10) which is in agreement with findings of Ahmadivand et al, 2014 [1] with a similar study on the histopathological response of male trout subjected to butachlor. These findings may be attributed to the fact that kidneys are the main organs responsible for excretion and also due to residual accumulation of pesticide in the kidney tissue as mentioned by California EPA (2001a) [8] .…”
Section: Catalase (Cat)supporting
confidence: 89%
“…[3] in deltamethrin and cypermethrin treated rats respectively. [Table 06] [1] with a similar study on the histopathological response of male trout subjected to butachlor. These changes may be due to the organ responsible for detoxification of the pesticide which receives massive amounts of metabolites and also due to residual accumulation of it as mentioned by Black et al, 1994 [7] who mentioned that chlorfenapyr acquires insecticidal properties after metabolic activation which functions as un-coupler of oxidative phosphorylation in mitochondria.…”
The experiment was carried out to evaluate the rising concern over additive effect of one chemical with another chemical which have raised a lot of health concern in general population. In the experiment, adult wistar rats of either sex were divided into 4 groups and study was conducted for a period of 28 days. Group I served as control and was provided with water only for drinking purposes. Animals of group II were administered butachlor@262mg/kg B.W/P.O. Group III recieved administered lead acetate@265ppm orally while animals of group IV received combination of butachlor@262mg/kg and lead acetate@265ppm. Oxidative stress was revealed by significant increase in lipid peroxidation and decrease in blood glutathione, glutathione peroxidase and transferase, catalase and superoxide dismutase in blood and tissues respectively. Histopathologically, liver and and kidney exhibited structural alterations as compared to control. The study concluded butachlor and lead produced more deleterious systemic effect in combination than alone (additive toxic effect).
“…Group III animals administered with lead acetate @265ppm exhibited mild congestion with tubular degeneration (Plate 9). Kidney section of rats of group IV co-administered with butachlor @262mg/kg and lead acetate @265ppm showed moderate degeneration of epithelial cells of PCT, hypercellularity of glomeruli, and presence of intra tubular hyaline cast (Plate 10) which is in agreement with findings of Ahmadivand et al, 2014 [1] with a similar study on the histopathological response of male trout subjected to butachlor. These findings may be attributed to the fact that kidneys are the main organs responsible for excretion and also due to residual accumulation of pesticide in the kidney tissue as mentioned by California EPA (2001a) [8] .…”
Section: Catalase (Cat)supporting
confidence: 89%
“…[3] in deltamethrin and cypermethrin treated rats respectively. [Table 06] [1] with a similar study on the histopathological response of male trout subjected to butachlor. These changes may be due to the organ responsible for detoxification of the pesticide which receives massive amounts of metabolites and also due to residual accumulation of it as mentioned by Black et al, 1994 [7] who mentioned that chlorfenapyr acquires insecticidal properties after metabolic activation which functions as un-coupler of oxidative phosphorylation in mitochondria.…”
The experiment was carried out to evaluate the rising concern over additive effect of one chemical with another chemical which have raised a lot of health concern in general population. In the experiment, adult wistar rats of either sex were divided into 4 groups and study was conducted for a period of 28 days. Group I served as control and was provided with water only for drinking purposes. Animals of group II were administered butachlor@262mg/kg B.W/P.O. Group III recieved administered lead acetate@265ppm orally while animals of group IV received combination of butachlor@262mg/kg and lead acetate@265ppm. Oxidative stress was revealed by significant increase in lipid peroxidation and decrease in blood glutathione, glutathione peroxidase and transferase, catalase and superoxide dismutase in blood and tissues respectively. Histopathologically, liver and and kidney exhibited structural alterations as compared to control. The study concluded butachlor and lead produced more deleterious systemic effect in combination than alone (additive toxic effect).
“…; Ahmadivand et al . ). However, according to Camargo & Martinez , to some extent, such changes can be explained as an organism defence response, when the distance between the blood circulatory system and the external environment increases due to the occurrence of a stress‐inducing substance.…”
Section: Discussionmentioning
confidence: 97%
“…Particularly worrying are the structural changes observed at the highest KYNA concentration (250 mg kg À1 ), including fusion or disappearance of gill lamellae. Comparable changes have been documented in the case of pesticides, heavy metals, chitosan or in fish living in urban water (Bullock et al 2000;Camargo & Martinez 2007;Boran et al 2012;Ahmadivand et al 2014). However, according to Camargo & Martinez 2007, to some extent, such changes can be explained as an organism defence response, when the distance between the blood circulatory system and the external environment increases due to the occurrence of a stress-inducing substance.…”
Kynurenic acid (KYNA) is an endogenous substance produced on the kynurenine pathway which is primarily known for its neuroactive properties. Recently, it has been proven that KYNA is a selective ligand for G protein-coupled receptor (GPR 35), presented on immunocompetent cells such as T lymphocytes. This opens up new possibilities of its application as an immunostimulating substance in aquaculture. Thus far, no histopathological investigations in fish have been completed to evaluate influence of KYNA supplementation in feed. This study has been undertaken to determine the effect of feed supplementation with KYNA (2.5, 25, 250 mg kg of feed) for 28 days on the liver, gills and kidney in healthy fish and experimentally infected with Yersinia ruckeri. In a control group were observed a fatty liver, which is natural for this fish species in the autumn and winter season. As the dose of the supplement was increased, the fat liver changed, it decreased or completely disappeared. Additionally, inflammatory changes occurred in all the analysed organs, and their intensification was dose dependent. In the fish experimentally infected, KYNA caused aggravation of the signs in the liver, kidneys and gills, and the effect was dose dependent. The results implicate that KYNA may be a stressor for fish.
“…Histopathological examination is a sensitive procedure for assessing cellular impairment in the organ of an animal following their expose to xenobiotics (Ayoola and Ajani, 2008). Fish exposed to pollutants have been reported to display various pathological conditions in different organs such as liver, kidney and gill after their exposure to toxicants (Ahmadivand et al, 2014). The gill of fish is capable of absorbing toxicants with the gill filaments and lamellae being the most important site of the action of xenobiotics in the gill.…”
Chlorpyrifos (CPF) is a very toxic pesticide commonly used for controlling agriculturally important pests. The present study investigates DNA damaging effects of CPF on Clarias gariepinus was assessed using genetic assays. Fish were exposed to varying concentrations of CPF (100ppm, 200ppm and 300ppm) at 96 hours (acute exposure). LC50 of the pesticide was found to be 120ppm and one-tenth of the LC50 (12ppm) was taken for the chronic exposure. Distilled water and colchicine were used as negative and positive controls respectively. After 28 days of chronic exposure, fish were fed with inclusion of B. sapida seed (powder) for 14 days. Liver and gills of the fish were removed following 96h exposure, days 7, 14 and 28 of the chronic exposure as well as after the period of amelioration (14 days) for CA assay and histopathological analysis. The results of CA assay showed statistically significant (p ˂ 0.05) increase in CA in a dose-dependent manner for all the exposed groups after acute exposure and time dependent after chronic exposure. Also, this study showed that CPF can potentially induce genotoxic and histopathological changes in fish and other aquatic organisms.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.