Teratological effects of Dimethoate on 12th day desi chick embryo (Gallus gallus domesticus).
Dimethoate ([C.sub.5][H.sub.12]N[O.sub.3]P[S.sub.2]) is a highly stable compound and partially decomposes even at extremely higher temperature. It is widely used organophosphate to control insect pests in agricultural and non-agricultural areas (Farag et al., 2007). The main mode of action is the inhibition of acetylcholinesterase (AChE) enzyme in the nervous system. This enzyme stimulates the hydrolysis of acetylcholine in cholinergic synapses. Inhibition of AChE leads to an accumulation of the neurotransmitter, causing overstimulation of cholinergic receptors (Guilhermino et al., 1996; Payne et al., 1996), neuromuscular paralysis and uncoordinated movements which can result in the organism's death (Howcroft et al., 2011). Dimethoate residues persist in the surrounding environment, and affects non target organisms like the domestic chicken. Moreover, its residues on soil, commercial feed and ingredients are potential routes of exposure to domestic birds. Dimethoate is highly toxic to birds, as its residues persist in their tissues (Ahmad et al., 2010; Botella et al., 2004). Whereas, developing chick embryos are more vulnerable than adults, because their immune system, detoxifying enzymes, liver metabolism, and the blood brain barrier are not completely developed (Alhifi, 2011; Newbold et al., 2007).
Poultry is a rich source of cheap, palatable nutritious protein and a constituent of our daily food in the form of eggs and white meat (Ghafoor et al., 2010). In subcontinent (Pakistan and India), farmers rear local poultry breeds to fulfill meat requirements (Kumaresa et al., 2008). Poultry meat is a good substitute for beef and mutton (Tufail et al., 2012). In Pakistan, more than 79.6 million rural poultry birds, contribute 32% and 15% of the egg and meat production, respectively (Memon, 2013). Desi chicken (Gallus gallus domesticus) is a common domestic fowl, belonging to the Phasianidae family (Perrins and Buffalo, 2003). It is a good and delicious source of meat and eggs, and alternative income among the households in the rural areas (Lingaya et al., 2007). However, its production is least compared to market demands in the country. The hazardous chemicals in the environment, poor reproductive potentials and lack of genetically improved indigenous breeds are mainly responsible for this low production. Insecticides, met als and fungicides cause morphological and histopathological abnormalities, biochemical changes, organ dysfunction and mortality in the young embryos (Anwar, 2003).
Previously, many authors documented the toxicity of dimethoate on broilers, mammals, aquatic and soil inhabiting organisms (Paithane et al., 2012; Farag et al., 2011; 2007; Juhasz et al., 2005; Budai et al., 2001; Varnagy et al., 2001). However, there is dearth of literature on the toxicological and morphological impact of dimethoate on 'desi' chicks (Budai et al., 2003; .Varnagy et al., 2001). Therefore, the present study was designed to investigate the embryotoxic and teratogenic effects of dimethoate on the early developmental stages of 'desi' chicks (G. gallus domesticus).
Materials and Methods
In the present study, toxicity of commercial formulation of dimethoate (38% EC) insecticide was evaluated on 'desi' chick embryos (G. gallus domesticus). The experiment was conducted in the Developmental Biology Laboratory, Department of Zoology, University of Gujrat, Gujrat, Pakistan. A total of 150 fertilized eggs were purchased from local breeders of Chak Sada, Gujrat. These eggs were divided randomly into 5 groups (n=30 in each group) irrespective of their size and colour and treated with 5 different concentrations (0, 0.3, 0.6, 0.9 and 1.2% 100 [micro]L/egg), 0 concentration without dimethoate was used as control. Dimethoate (38% EC), Pakistan Agro-Chemicals (pvt.) Ltd. was purchased from a local pesticide vendor. The required concentrations were obtained by serial dilution of 4% fresh stock solution with acetone.
A small hole was made in the shell of each egg (experimental groups) by using dissecting needle avoiding the membrane to rupture. A single dose (100 [micro]L) of each concentration was injected horizontally into the yolk sac of each respective group with a micro applicator (1 inch long no. 27). The hole in the shell was sealed with adhesive tape after treatment. In order to avoid contamination, the eggs injected were in a room with a sterile atmosphere.
The shelves of the incubator (100-800 Memmert) were covered by a layer of cotton, to avoid direct contact of eggs with shelf surface. All the eggs were placed in incubator, in such a way that broader ends remains upward, at the optimum temperature of 38 [+ or -] 0.5 [degrees]C, relative humidity of 60% and ventilator was made open. The eggs were rotated after every 8 h of incubation throughout the experiment, candled on daily basis and dead embryos were culled out.
The recoveries were made at the 12th day of incubation. The eggs were opened by cracking and albumin was removed with the help of blunt forceps. The embryos were separated from yolk in a petri dish containing water and examined for malformations. These malformations were observed with a magnifying lens and also with naked eye. The wet body weight of the embryos was measured at an analytical balance (Shimadzu AY120) and they were examined for the presence of any external malformations. Measurements of crown-rump length, head (anterior-posterior) diameter, eye diameter, neck, and beak were done by a caliper while fore limbs (humerus, radius, and metacarpus) and hind limbs (femur, fibula and metatarsus) were done with the help of a scale and a compass. Embryos were photographed and mortality rate was recorded.
Statistical Analysis: The data was analysed statistically by analysis of variance of linear model followed by LSD using the statistical software Statistix 8.1. Values were expressed as Mean [+ or -] SE and differences between control and treated groups were considered significant when P< 0.05 (Bolton, 1997).
Results and Discussion
Table 1 represents the mortality rate of 'desi' chick embryos treated with different concentrations of dimethoate. The mortality rate of chick embryos is directly proportional to the dose concentration of insecticide (Pourmirza, 2000). In the current study, embryotoxic severity of dimethoate was found dose dependent and the mortality rate was increased gradually from the application of lower to higher concentration. Hence, most of the embryos (76.66%) were found not viable, when treated with 1.2% concentration. While only 10% embryos were found dead in the control group. Various factors might be responsible for the embryos death in the control group such as air hunger, quality of the eggs, genetic factor, breed, pathological conditions, lack of proper hygiene and position of the egg during incubation and orientation of the primitive streak also play crucial role in the viability of embryos (Kalita et al., 2013; Byerly and Olsen, 1931). Juhasz et al. (2005) and Budai et al. (2003) in their individual experiments studied the embryotoxic effect of dimethoate and heavy met al load of the environment on the early phase of chick development. They separately confirmed the toxicity of dimethoate on the developing embryos. Further, they added that presence of heavy met als in the environment might be more hazardous for embryonic development.
Table 2 shows the measurements of morphometric parameters. 'Desi' chick embryos treated with different concentrations of dimethoate showed reduction in the wet body weight, crown rump length, anterior posterior head diameter, eye diameter, beak, humerus, radius, metacarpus, femur, fibula and metatarsus length compared to control group. The malfunctioning of these structures increased with the increase in concentration of dimethoate, therefore, at low concentration, some body structure e.g. humerus, radius and fibula did not show significant difference (P < 0.05) to control group. The maximum malfunctioning was found in wet body weight, crown rump and metacarpus length and had significant difference (P < 0.05) compared to control group. These results are in accordance with Keseru et al. (2004) and Budai et al. (2001). They independently documented that, dimethoate has hazardous impact on the developing embryos, and abnormal development appear more significant at higher concentrations. Irrespective of early developmental stages, dimethoate also has deleterious effect on adults too. For instance, in female rats, it caused the reduction of body and kidneys weight (Farag, 2007). Many authors documented various malformations in broiler chick embryos with dimethoate and other formulations, e.g. reduction in limbs, microcephaly and body weight (Lenselink et al., 1992) and reduced crown rump length and body weight by the application of metasystox-R and methyl parathion, respectively (Sunil and Devi, 1992). Chlorpyrifos, cypermethrin, spinosad, malathion and endosulfan also have similar effects on different organs during embryonic development (Mobarak and Al-Asmari, 2011; Uggini et al., 2010; Anwar, 2003; Pourmirza, 2000). Furthermore, Sepulveda et al. (2006) and Singh et al. (2007) described malformations in different body structures in alligator and rat embryos when exposed to citrinin, endosulfan and organochlorine insecticides.
Various anomalies in 'desi' chick embryos were recorded by the application of different concentrations of dimethoate (Table 3). Anomalies also gave similar trends like the impact on different organs treated with insecticide as described earlier. Fourteen different anomalies were recorded, of which agnathia, microcepahaly, microphthalmia, anophthalmia, short neck and omphalocelle showed gradual increase in the percentage anomalies with the treatment of low to higher concentration of insecticide and observed with all applied concentrations. However, abnormal colouration (04.34%) was recorded only with treatment of low concentration (0.30%) insecticide, while, micromelia and amelia only appeared with treatment of 0.9 and 1.2% concentration of dimethoate. Figure 1(a-h) shows the control group embryo, and dimethoate treated embryos that were examined on embryonic day 12th, exhibited one type or 24 types of malformations with different concentrations of dimethoate (0.30%, 0.60%, 0.90% and 1.2%). Anomalies exhibit a periodic trend as described by Morale et al. (1998) and Mobarak and Al-Asmari (2011) in contrast to Varnagy et al. (2001) and Budai et al. (2003). They suggested sporadic manner. Similar results have been documented by a number of authors (Mobarak, 2009; Ahmad and Asmatullah, 2007; Anwar, 2003; Asmatullah et al. 2002). Gilbertson et al. (1991) observed subcutaneous, pericardial and peritoneal edema in fish-eating birds, exposed to insecticide contaminants. Whereas, Fry (1995) and Guiney et al. (1997) documented pericardial edema, severe and generalised vascular damage in lake trout and zebrafish on pesticides (DDT, PCB, 2, 3, 7, 8-tetrachloro-p-dioxin) exposure at early developmental stages.
[FIGURE 1 OMITTED]
It is concluded from the present study that dimethoate has adverse effects on the development of 'desi' chick embryos. Whereas, due to its stability at higher temperature, enable this compound to persist for longer times in the surrounding environment. Therefore, this insecticide might be harmful for farm animals and human. Hence, further studies are needed to evaluate the concentrations level in the environment and impact on other domestic animals and human etc.
Ahmad, K.R., Asmatullah. 2007. Teratological effects of chlorpyrifos in mice. Iranian Journal of Toxicology, 1: 91-99.
Ahmad, R., Salem, N.M., Estaitieh, H. 2010. Occurrence of organochlorine pesticide residues in eggs, chicken and meat in Jordan. Chemosphere, 78: 667-671.
Alhifi, M.A. 2011. Effect of pesticides mixture of dimethoate and methidathion on acetylcholinestrase during embryo development using chick embryo model. Egyptian Academic Journal of Biological Science, 3:19- 26.
Anwar, K. 2003. Cypermethrin, a pyrethroid induces teratological and biochemical changes in young chick embryos. Pakistan Journal of Biological Science, 6: 1698-1705.
Asmatullah, Jabeen, Z., Andaleeb, S. 2002. Embryotoxic effects of fenvalerate in developing chick. Punjab University Journal of Zoology, 17: 126-133. Bellairs, R., Osmond, M. 1998. The Atlas of Chick Development. vol. 3, pp. 215-223, Academic Press, New York, USA.
Bolton, S. 1997. Nonparametric methods. In: Pharmaceutical Statistics, pp. 537-588,3rd edition, J. Swarbrick (ed), Mercel Dekker, Inc., NY, USA.
Botella, B., Crespo, J., Rivas, A., Cerrillo, I., Olea-Serrano, F., Olea, N. 2004. Exposure of women to organochlorine pesticides in southern Spain. Environmental Research, 96: 34-40.
Budai, P., Fejes, S., Varnagy, L., Somlyay, I.M., Szabo, Z.K. 2003. Teratogenicity test of dimethoate containing insecticide formulation and Cd-sulphate in chicken embryos after administration as a single compound or in combination. Communication in Agricultural and Applied Biological Science, 68: 795-798.
Budai, P., Fejes, S., Vamagy, L., Somlyay, I.M., Takacs, I. 2001. Teratogenicity test of dimethoate containing insecticide formulation and heavy elements (Cu, Cd) in chicken embryos after administration as single compound or in combination. Meded Rijksuniv Gent Fak Landbouwkd Toegep boil Wet, 66: 885-889.
Byerly, T.C., Olsen, M.W. 1931. The influence of gravity and air-hunger on hatchability. Poultry Science, 10: 281-287.
Farag, A., Ebrahim, H., El Mazoudy, R., Kadous, E. 2011. Development toxicity of fungicide carbendazim in female mice. Birth Defect Research, (Part B) 92: 122-130.
Farag, A.T., Al-aswad and Shaaban, A.N. 2007. Assessment of reproductive toxicity of orally administered technical dimethoate in male mice. Egypt Reproductive Toxicology, 23: 232-238.
Fry, D.M. 1995. Reproductive effects in birds exposed to pesticides and industrial chemicals. Environmental Health Perspectives, 103: 165-171.
Ghafoor, A., Badar, H., Hussain, M., Tariq, N. 2010. An empirical estimation of the factors affecting demand and supply of poultry meat. Pakistan Veterinary Journal, 30: 172-174.
Gilbertson, M., Kublak, T., Ludwig. J., Fox, G. 1991. Great Lakes embryo mortality, edema and deformities syndrome (GLEMEDS) in colonial fish-eating birds: Similarity to chick-edema disease. Journal of Toxicology and Environmental Health, 33: 455-520.
Guilhermino, L., Lopes, M.C., Carvalho, A.P., Soared, A.M.V.M. 1996. Inhibition of acetylcholinesterase activity as effect criterion in acute tests with juvenile Daphniamagna. Chemosphere, 32: 727-738.
Guiney, P.D., Smolowitz, R.M., Peterson, R.E., Stegeman, J. J. 1997. Correlation of 2,3,7, 8-tetrachloro-p-dioxin induction of cytochrome P4501A in vascular endothelium with toxicity in early life stages of lake trout. Toxicology and Applied Pharmacology, 143: 256-273.
Henry, T. R., Spitsbergen, J.M., Hornung, M.W., Abnet C.C., Peterson, R.E. 1997. Early life stage toxicity of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin in zebrafish (Danio rerio). Toxicology and Applied Pharmacology, 142: 56-68.
Howcroft, C.F., Gravato, C., Amorim, M.J.B., Novais, S.C., Soares, A., Guilhermino, L. 2011. Biochemical characterization of cholinesterases in Enchytraeus albidus and assessment of in vivo and in vitro effects of different soil properties, copper and phenmedipham. Ecotoxicology, 20: 119-130.
Juhasz, E., Szabo, R., Keseru, M., Fejes, S., Budai, P., Kertesz, V., Varnagy, L. 2005. Early embryogenesis study on a dimethoate containing formulation and Cd-sulphate in chicken embryos. Communication in Agricultural and Applied Science, 70: 10751078.
Kalita, N., Pathak, N., Ahmed, M., Saikia, G.K. 2013. Various causes related to dead-in-shell embryos of crossbred (PB-2 x Indigenous) chicken egg. Veterinary World, 6: 774-777.
Keseru, M., Budai, P., Varnagy, L., Szabo, R., Juhasz, E., Babinszky, G., Pongracz, A. 2004. Teratogenicity study of some pesticides in chicken embryos. Communication in Agricultural and Applied Science, 69: 803-806.
Kumaresa, A., Bujarbarun, K.M., Pathak, K.A., Chhetri, B., Ahmed, S.K., Haunshi, S. 2008. Analysis of a village chicken production system and performance of improved dual purpose chickens under a sub tropical hill agro-ecosystem in India. Tropical Animal Health and Production, 40: 395-402.
Lenselink, D.R., Midtling, J.E., Lawrence, J.M., Kolesari, G.L. 1992. Teratogenic effects of metasystox-Rinthe stage 12 chick embryo. Teratology, 45: 500-501.
Lingaya, R.A.I.N., Oliveros, M.C.R., Magpantay, V.A. 2007. Production performance and marketing of native chicken in the first and fourth districts of Iloilo. Philippine Journal of Veterinary and Animal Sciences, 33: 163-171.
Memon, N.A. 2013. Poultry: Country's Second-largest Industry. pp. 27-30, Ministry of National Food Security & Research, Pakistan.
Mobarak, Y.M., Al-Asmari, M.A. 2011. Endosulfan impacts on the developing chick embryos: morphological, morphometric and skelet al changes. International Journal of Zoological Research, 7: 107-127.
Mobarak, Y.M. 2009. Embryoprotective efficacy of Rosmarinus officinalis (Rosemary) extract against developmental toxicity and teratogenicity of mercuric chloride in the chick. Egyptian Journal of Zoology, 52: 67-91.
Morale, A., Coniglio, L., Angelini, C., Cimoli, G., Bolla, A., Alleteo, D. 1998. Biological effects of a neurotoxic pesticide at low concentrations on sea urchin early development: a teratogenic assay. Chemosphere, 37: 3001-3010.
Newbold, R.R., Padilla-banks, E., Snyder, R.J., Phillips T.M., Jefferson, W.N. 2007. Developmental exposure to endocrine disruptors and the obesity. Epidemic Reproductive Toxicology, 23: 290-296.
Paithane, K. T., Sonawane, D.L., Bandare, R.Y., More, P.R. 2012. Histopathological changes due to induced Dimethoate in the liver of freshwater fish Channa punctatus from river Shivana, Aurangabad India. An International Quarterly Journal of Environmental Sciences, 1:213-217.
Payne, J.F., Mathieu, A.W.M., Fancey, L.L. 1996. Acetylcholinesterase, an old biomarker with a new future? Field trials in association with two urban rivers and a paper mill in Newfoundland. Marine Pollution Bulletin, 32: 225-231.
Perrins, E., Buffalo, C. 2003. According to Firefly Encyclopedia of Birds, vol. 3, pp.34-37, Firefly Books, Ltd., USA.
Pourmirza, A. A. 2000. Toxic effects of malathion and endosulfan on chick embryo. Journal of Agricultural Science and Technology, 2: 161-166.
Sepulveda, M.S., Del Pietro, F., Wiebe, J.J., Rauschenberger, H.R., Gross, T.S. 2006. Necropsy findings in American alligator late-stage embryos and hatchlings from north-central Florida lakes contaminated with organochlorine pesticides. Journal of Wildlife Diseases, 42: 56-73.
Singh, N. D., Sharma, A.K., Dwivedi, P., Patil, R.D., Kumar, M. 2007. Citrinin and endosulfan induced teratogenic effects in Wistar rats. Journal of Applied Toxicology, 27: 143-151.
Sunil, K.B., Devi, K.S. 1992. Teratogenic effect of methyl parathion in developing chick embryos. Veterinary and Human Toxicology, 34: 408-410.
Tufail, M., Sajjad, M., Zulfiqar, M., Sohail, S.M., Ahmad, I. 2012. Economic of backyard poultry in tehsil Matta, district Swat. Sarhad Journal of Agriculture, 28: 485-492.
Uggini, GK., Patel, P.V., Balakrishnan, S. 2010. Embryotoxic and teratogenic effects of pesticides in chick embryos: A comparative study using two commercial formulations. Environmental Toxicology, 5: 1-9.
Varnagy, L., Budai, P., Molnar, E., Fuzesi, I., Fancsi, T. 2001. Teratogenicity testing of BI 58 EC (38% dimethoate) in chicken embryos with special respect to degradation of the active ingredient. Acta Veterinaria Hungarica, 49: 355-361.
Shamila Sabir (a), Muhammad Sajjad Ansari (a), Muhammad Nadeem Abbas (a) *, Razia Iqbal (a), Javed Iqbal (b), Saima Kausar (c) and Sadaf Chaudhary (a)
(a) Department of Zoology, University of Gujrat, Hafiz Hayat Campus, Gujrat, Pakistan (b) Punjab Group of Colleges, 64 El Gulberg III, Lahore, Pakistan
(b) Department of Zoology and Fisheries, University of Agriculture, Faisalabad, Pakistan
(received May 5, 2014; revised October 12, 2015; accepted October 30, 2015)
* Author for correspondence; E-mail: email@example.com
Table 1. Embryos mortalities of dimethoate treated and control group of 'desi' chicken eggs (n=30 each group) Treatment Dose /egg (%) dead embryo (n) Mortality (%) Control -- 3 10.00 Dimethoate 0.3 7 23.33 0.6 12 40.00 0.9 19 63.33 1.2 24 76.66 Table 2. Mean [+ or -] SE % of morphometric values of untreated and dimethoate treated 'desi' chick embryos Treatment groups Parameters Control Wet body weight (g) 5.72 [+ or -] 0.12 (a) C.R length (cm) 5.22 [+ or -] 0.11 (a) A.P head diameter (cm) 1.58 [+ or -] 0.03 (a) Eye diameter (cm) 1.00 [+ or -] 0.01 (a) Beak length (cm) 1.31 [+ or -] 0.03 (a) Neck length (cm) 0.96 [+ or -] 0.02 (a) Humerus length (cm) 0.91 [+ or -] 0.02 (a) Radius and ulna length (cm) 0.87 [+ or -] 0.02 (a) Metacarpus length (cm) 0.85 [+ or -] 0.01 (a) Femur length (cm) 1.35 [+ or -] 0.02 (a) Fibula length (cm) 1.11 [+ or -] 0.02 (a) Metatarsus length (cm) 1.00 [+ or -] 0.02 (a) Treatment groups Parameters 0.30% Wet body weight (g) 5.30 [+ or -] 0.14 (b) C.R length (cm) 4.71 [+ or -] 0.14 (b) A.P head diameter (cm) 1.46 [+ or -] 0.04 (ab) Eye diameter (cm) 0.98 [+ or -] 0.02 (ab) Beak length (cm) 1.28 [+ or -] 0.03 (a) Neck length (cm) 0.93 [+ or -] 0.03 (ab) Humerus length (cm) 0.90 [+ or -] 0.02 (a) Radius and ulna length (cm) 0.84 [+ or -] 0.03 (ab) Metacarpus length (cm) 0.78 [+ or -] 0.01 (b) Femur length (cm) 1.29 [+ or -] 0.03 (ab) Fibula length (cm) 1.06 [+ or -] 0.03 (ab) Metatarsus length (cm) 0.90 [+ or -] 0.02 (b) Treatment groups Parameters 0.60% Wet body weight (g) 4.77 [+ or -] 0.14 (c) C.R length (cm) 4.22 [+ or -] 0.13 (c) A.P head diameter (cm) 1.39 [+ or -] 0.04 (bc) Eye diameter (cm) 0.93 [+ or -] 0.02 (b) Beak length (cm) 1.26 [+ or -] 0.03 (a) Neck length (cm) 0.87 [+ or -] 0.03 (b) Humerus length (cm) 0.89 [+ or -] 0.02 (ab) Radius and ulna length (cm) 0.82 [+ or -] 0.03 (ab) Metacarpus length (cm) 0.70 [+ or -] 0.01 (c) Femur length (cm) 1.26 [+ or -] 0.03 (b) Fibula length (cm) 1.00 [+ or -] 0.03 (bc) Metatarsus length (cm) 0.80 [+ or -] 0.02 (c) Treatment groups Parameters 0.9% Wet body weight (g) 4.12 [+ or -] 0.13 (d) C.R length (cm) 3.83 [+ or -] 0.13 (d) A.P head diameter (cm) 1.30 [+ or -] 0.04 (c) Eye diameter (cm) 0.86 [+ or -] 0.02 (c) Beak length (cm) 1.14 [+ or -] 0.03 (b) Neck length (cm) 0.86 [+ or -] 0.02 (b) Humerus length (cm) 0.82 [+ or -] 0.02 (b) Radius and ulna length (cm) 0.76 [+ or -] 0.03 (bc) Metacarpus length (cm) 0.65 [+ or -] 0.01 (d) Femur length (cm) 1.11 [+ or -] 0.02 (c) Fibula length (cm) 0.96 [+ or -] 0.02 (cd) Metatarsus length (cm) 0.73 [+ or -] 0.02 (d) Treatment groups Parameters 1.2% Wet body weight (g) 3.41 [+ or -] 0.13 (e) C.R length (cm) 3.33 [+ or -] 0.12 (e) A.P head diameter (cm) 1.11 [+ or -] 0.04 (d) Eye diameter (cm) 0.78 [+ or -] 0.02 (d) Beak length (cm) 0.97 [+ or -] 0.03 (c) Neck length (cm) 0.77 [+ or -] 0.02 (c) Humerus length (cm) 0.73 [+ or -] 0.02 (c) Radius and ulna length (cm) 0.68 [+ or -] 0.03 (c) Metacarpus length (cm) 0.60 [+ or -] 0.01 (e) Femur length (cm) 1.02 [+ or -] 0.02 (d) Fibula length (cm) 0.90 [+ or -] 0.02 (d) Metatarsus length (cm) 0.60 [+ or -] 0.02 (e) Means with different superscripts differ in sign in a row: Values expressed as mean; P < 0.05; a-e marked on different rows refer to the significant difference with each other and to control. Table 3. Frequency percentages of particular anomalies observed in dimethoate treated 'desi' chick embryos Anomalies Treated embryos 0.30% 0.60% 0.9% 1.2% Agnathia 08.69 11.11 18.18 28.57 Microcephaly 04.34 05.55 18.18 28.57 Abnormal colouration 04.34 - - - Microphthalmia 04.34 11.11 18.18 28.57 Anophthalmia 04.34 05.55 09.09 14.28 Hematoma 04.34 16.66 09.09 14.28 Meromelia 08.69 11.11 18.18 - Edema 17.39 05.55 09.09 14.28 Short neck 04.34 11.11 18.18 14.28 Omphalocelle 04.34 05.55 09.09 14.28 Micromelia - - 27.27 42.85 Exencephaly - 11.11 18.18 - Amelia - - 18.18 14.28 Twisted beak - 05.55 - 14.28
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|Author:||Sabir, Shamila; Ansari, Muhammad Sajjad; Abbas, Muhammad Nadeem; Iqbal, Razia; Iqbal, Javed; Kausar,|
|Publication:||Pakistan Journal of Scientific and Industrial Research Series B: Biological Sciences|
|Date:||Nov 1, 2015|
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