ALLETHRIN Toxbase summary Toxicity Dermal and inhalational exposures are . “supernormal period” is the period for which the action potential induced by a. They are not considered to cause delayed neurotoxicity of the kind induced by some organophosphorus compounds. The mechanism of toxicity of synthetic. Allethrin had 96 h LC50 toxicity values of µg/L, µg/L > µg/L, and .. is followed by induction of microsomal oxidase activity (Škrinjarič-Špoljar et al.
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The datasets, supporting the conclusions of the results of this study are alelthrin within the article. The authors will be obedient to supply the raw data upon request. Mosquito coil MC emits insecticide upon burning which provides limited protection against lethal mosquito borne diseases. However, apart from killing the insect, toxicities associated with the inhalation of these insecticides poses severe health hazards.
However, the use of MC is increasing day by day in third world countries in particular but, yet to receive enough attention of both policy maker and general public. The current study was aimed to assess the MC smoke induced damage of pulmonary and hepatic tissues along with observing the alterations of several blood biochemical parameters in mice model. By the end of treatment period, blood alllethrin was drawn from each mouse and blood biochemical parameters including alanine imduced ALTaspartate transaminase ASTblood urea nitrogen BUNserum total protein, cholesterol, low density lipoprotein LDL and triglyceride TG were analyzed.
Intact onduced and liver were collected for histological analysis using standard protocol. Biochemical study indicates elevated activity of two hepatic enzymes: Pulmonary tissue of treated mice shows severe forms of emphysema and hyperplasia, especially in the peripheral region of lung, which is the hallmark of chronic obstructive toxkcity disease COPD.
Histological study of hepatic tissue shows apoptosis mediated damage of hepatocytes along with severe form of necrosis. Infiltration of Inflammatory cells was also observed in both of the organs. Results from the present studies suggest that chronic exposure of allethrin based MC is responsible factor for severe health complications such as COPD due to the alterations of the key biochemical parameters of blood and histo-organization of lung and liver.
Mosquito toxicitj is the slow-burning structure made mainly of insecticides along with inert materials such as wood floor, coconut shell powder, starch iinduced. Upon burning, MC emits smokes, containing single or multiple insecticides, which creates a defending environment and protects the subject from several mosquito borne lethal diseases including malaria, filaria and dengue.
Pyrethroids and Pyrethrins are the main active ingredients of MC. Among otxicity several types of pyrethroid, allethrin especially d-transallethrin belong to the type I pyrethroids is being used in almost all brands of mosquito coil in Inducwd Asian territory. On the other hand pyrethroids have well been reported to induce oxidative stress and alter antioxidant level in different organ systems of rodent animal [ 23 ].
MC smoke is considered as a potent air pollutant in indoor environment. One MC, upon burning, produces such amount of particulate matter equivalent to that of 75— cigarettes [ 4 ].
Along with insecticides, MC smoke also contains sub-micrometer particles, volatile, semi-volatile organic compounds and gaseous pollutants such as polyaromatic hydrocarbons [ 56 ]. After using the MC in a room, it was observed that the maximum concentration of allethrin 0. During overnight burning, subjects at close proximity are exposed to sub-micrometer particles, metal fumes, free radicals and vapors from smoke which ultimately reaches the alveolar region of lung and ijduced to irritation of the upper respiratory tract [ 6 ].
Chronic inhalation of MC smoke has been reported to correlate with asthma and persistent wheeze in human [ 8 ] along with focal declination and metaplasia in tracheal epithelium in rodents [ 59 ]. Prolong exposure and subsequent entry of allethrin along with other MC derived particulate matters into red blood cells lead to the alteration of blood biochemical parameters including hemoglobin percentages [ 1011 ].
Exposure of pyrethrin based MC smoke has also been reported to considerable increase in white blood cell WBCespecially basophil and lymphocyte in rat [ 12 ]. This noxious synthetic chemical is proven to be responsible for alletthrin, tissue and organs injury due to exerting its action on allethrin membrane phospholipids, resulting membrane fluidity and tissue damage [ 1113 ].
The toxic smoke, emitted from MC is also reported to be responsible for inducing chromosomal aberrations in pulmonary alveolar macrophages and bone marrow [ 1415 ]. Recently, Madhubabu et al. Therefore, it could be postulated that MC smoke would induce apoptotic mediated tissue damage in subject with prolong exposure.
Subtropical climate, Poor drainage system and dense population are triggering the mosquito pressure day by day in tropical region including Bangladesh. As a cheap and instant remedy, middle and lower income groups are regularly using MC. Thus, a huge number of people are undesirably exposing to toxic fine particles and free radicals present in the smoke of MC and are subjecting themselves to various health complications regularly [ 18 ].
Therefore, this study was aimed to analyze the patterns of damages in the histo-architecture of lung and liver tissues as well as the alteration of biochemical parameters of blood in mice model inhaled with the mosquito coil smoke. The animals were kept in the animal house of inducedd department of Biochemistry and Molecular Biology, University of Rajshahi, Bangladesh for acclimatization in the experimental environment.
Mosquito coil, used in this inducdd was purchased from local super market of Rajshahi by the trade name of Mortein power booster coil from Reckitt Benckiser, Bangladesh Ltd. The active ingredient of this brand was 0. Forty days old mice were randomly distributed into control and inhaled group: Control group six mice was allowed to receive normal air allethrinn separate chamber.
The inhaled group was then divided again into four subgroups each containing six mice: Inhalation treatment was conducted in limited ventilated space, creating a closed door setting mimicking the flat house. BUN level was estimated by enzymatic colorimetric method [ 20 ]. Serum total protein was measured by Biuret method, originally described by Josephson et al. Histological study was carried out using the protocol previously described by Carleton et al. In brief, at the ending of treatment period, animals from each group were anesthetized with diethyl-ether and sacrificed by cervical dislocation.
Intact lung and liver tissues were surgically removed quickly and washed with 0. Finally, the slides were visualized under light microscope optika, Italy and photographs were taken by the camera attached to it.
Descriptive statistical analysis was performed to estimate mean and standard deviation. The blood knduced, representing liver function, show significant changes in smoke inhaled groups in comparison with their respective control.
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Data indicates that the activity of two key hepatic enzymes i. Trends for p value indicates that when the treatments duration were increased, the activity of ALT, AST, cholesterol, LDL and triglyceride were increased as well as BUN and total protein concentration were decreased as a continuous variable. Taken together, the biochemical parameters were altered by the inhalation with the mosquito coil smoke in a dose-dependent manner. Pulmonary tissue of inhaled mice illustrates various degrees of histo-architectural changes in a doses dependent manner in comparison with that of control Fig.
Transverse section of lung of control mice shows normal and compact organization with thin intra-alveolar septa and alveolar sacs Fig. The ruptured alveoli further join with each other and form large air space especially in the peripheral region of lung Fig.
It implies that air ventilation through the bronchi and bronchiole in treated mice might be considerably reduced due to constricted bronchi CB in Fig.
Allethrins (EHC 87, )
Higher duration inhalation also resulted in pulmonary edema PE in Fig. Sections were stained with hematoxylin and eosin Original magnification, X Toxicological effects of MC smoke on hepatic tissue in control and smoke inhaled mice are shown in Fig. Microscopic observation of control liver shows regular and compact configuration with well-organized hepatocytes and central vein Fig. Toxiciry mice with higher duration of inhalation show degenerated hepatocytes DHdilation of central vein DC and dilation of sinusoid DS Fig.
CV indicates cytoplasmic vacuolation, CCA indicates condensation of cytoplasm of ongoing apoptotic cell, DH represents degeneration hepatocytes, ICI represents inflammatory cellular infiltration, DC indicates dilation of central vein, AC indicates apoptotic cells, NC indicates necrosis and DS is for dilation of sinusoid.
MC contains pyrethrin based insecticide but still widely being used in the tropical and subtropical region including Bangladesh as a common approach to protect mosquito from entering into home. MC generally has higher acceptance over liquid vaporizer due to its lower cost tocicity ease of use. Upon burning, MC releases over 60 organic compounds, fine and ultrafine particles and heavy metals [ 5 ]. The smoke is composed of two phases: During overnight burning, the smoke of particle phase allehrin carbon particles, heavy metals, aldehydes ultimately reaches peripheral region of lung and leading to progressive cellular injury and destruction of mucus membrane [ 9 ].
The present study demonstrates inducdd critical biochemical parameters of blood were altered significantly in MC smoke inhaled animals. Elevated activity of these hepatic enzymes is strongly correlated with hepatic injury [ 11 ]. Allethrin is membrane active substance, which acts upon membrane phospholipids and increases membrane fluidity [ 13 ] and leading to leak out cellular enzymes in extracellular matrix eventually increasing transaminases activity in blood.
Elevated transaminase level has also been reported previously by Karthikeyan et imduced. The exposure of MC smoke resulted dose dependent depletion of BUN and total protein activity in toixcity inhaled animals.
This finding is also supported by a number of observations which demonstrated that kidney functions were not negatively altered in MC smoke inhaled rat [ 511 ]. Similarly, the MC smoke has previously been reported to reduce serum total protein activity both in rodent animal and human subject [ 2728 ].
Higher protein degradation with subsequent reduction of total protein activity of blood in smoke inhaled subject has also been confirmed by marked increase of plasma free amino acid levels [ 28 ]. Elevated LDL activity is considered to be the risk factor for cardiac condition, because it transports cholesterol from the liver to peripheral tissues.
However, it is the first study that documented the raised cholesterol level in rodent animal treated with allethin based MC smoke via inhalation.
The oxidative damage, induced by ROS is the hallmark of cellular stress which modulates a number of signaling pathways including carcinogenesis, apoptosis, necrosis and inflammatory pathway. Free radical and volatile organic compounds present in the smoke of MC is considered as the potent contributor of oxidative DNA damage and tissue injury.
Under these stress conditions, the histological organization of pulmonary and hepatic tissues becomes affected which led to severe organ injury. Histological study of lung tissue demonstrates extensive destruction of the alveolar septa and bronchial epithelial wall resulting in loss of alveoli as well as capillary surface area. Thus, the current study shows the clear evidence of severe emphysema as a result of long time inhalation of allethrin based MC smoke Fig.
The key event of the development of emphysema is the imbalance between proteases and anti-proteases, which is well established [ 29 ]. The ROS, induced by MC smoke, interferes with the antioxidant defense system [ 16 ], which would triggers inflammatory response in damage sites [ 30 ]. Furthermore, over expression of p53 in MC induced animals [ indduced ] is also considered as the potent contributor of pulmonary and hepatic inflammation.
Under stress condition, p53 has been reported to activate pro-inflammatory cytokines at the site of stress induced pulmonary tissue in cigarette smoke inhaled rat [ allethron ]. However, the recruited inflammatory cells along with proteolytic enzymes act upon the anti-proteases collagen and elastin in alveolar region and inactivate them which in turn results in the destruction of alveolar septa and eventually develop emphysema [ 29 ].
Additional evidence has also confirmed the involvement of neutrophil in the degradation of elastin fibers with subsequent development of emphysema [ 32 ]. Emphysema in smoke inhaled animals is also accompanied by extensive thickening of alveolar septa and bronchial epithelial wall, which indicate hyperplasia over tissue growth.
Accumulation of inflammatory cells probably induces deposition of extracellular matrix in the sub epithelium region and contributes in thickening of bronchial epithelial wall [ 37 ]. The structure of epithelial lining of bronchi is converted from pseudo-stratified columnar ciliated epithelium into thickened constricted bronchi CB in fig-1C and 1Bwhich might limit air passing through the bronchi to the peripheral region of lung- major clinical feature in patient with COPD [ 38 ].
The activation of fibroblasts by inflammatory cells and with subsequent thickening of bronchial epithelial wall and alveolar septa are considered as airway resistance and airway remodeling against ongoing destruction of alveolar septa [ 37 ].
The co-existence alleyhrin necrotic and apoptotic mediated liver damage is the novel finding of this study AC and NC in Fig. Necrotic cells death characteristically affects large fields of tissue NC in figure- 2F rather than a single cell and induce to release cytoplasmic contents into the surrounding cellular alleghrin which leads to trigger inflammatory cells to be accumulated NC in Fig. Histological observation of hepatic tissue also reveals degeneration of hepatocytes in such a way, affecting single cell or small area of tissue without recruiting inflammatory cells: However, it is the first time study that we have observed apoptotic mediated cell death induced by the smoke of allethrin based MC.
Oxidative DNA damage with subsequent up-regulation of p53 is the perquisite of mitochondria mediated apoptosis [ 40 ]. The interplay between apoptosis and necrosis may take place at the same time in the same tissue depending upon the types and degrees of death stimuli [ 42 ], which would also be supportive to allethrin current dose dependent co-existence of apoptosis foxicity necrosis in smoke inhaled tissues.
This study has some limitations relating to the conclusion of the results.