Effect of Diclofenac Sodium in Broilers

Abstract

This study was conducted to determine the effects of diclofenac sodium in broiler chicks during the period from 20 th July /2012 to 1 st september/2012. The broiler chicks were divided into four groups A, B, C and control with ten day old bird in each. Group A was treated with @ 5mg/kg body weight, group B was treated with @ 10mg/kg body weight and Group C was treated with 20 mg/kg body weight given orally mixing with drinking water. Histopathological, hematological and biochemical tests were performed on 42 th days of age to evaluate diclofenac-induced changes between control and treated groups. Mortality rate and pathomorphological changes were observed in dead birds. The acute toxicity was assessed by observing the clinical signs and symptoms, mortality, alterations in blood biochemistry, and necropsy findings. The birds of Group A showed only mild symptoms of diarrhea and 30% mortality. In Group B, 60% and Group 70% of birds died in between 24 and 36 h post-treatment showing the symptoms of segregatory behavior, lethargy, terminal anorexia, and severe bloody diarrhea. Observation of hematological parameters like TEC, Hb, PCV and ESR on 42 th days of age showed significant (p<0.01) decrease in treatment group compare to control group. Observation of biochemical parameters (serum urea, serum creatinine) on 42 th days of age showed significantly increased (p<0.01) serum urea and serum creatinine indicating nephrotoxicity in broilers. At 12 and 24 h post-treatment this returned to the normal levels. The dead birds of the high-dose group also showed similar pattern of biochemical changes at 12 and 24 h post-treatment and revealed extensive visceral gout with characteristic histopathological lesions in liver, kidney, heart, spleen and intestine on post-mortem. The results indicate that diclofenac sodium has hepatotoxic, nephrotoxic, and visceral gout inducing potentials in broilers (cob-500), especially at higher dose.

The effect of diclofenac sodium on neural tube development in the early stage of chick embryos

“…For animals, 1-18 mg/kg DS doses were used in teratogenic studies related to pregnancy [3,6,19,44]. A toxic dose of DS was 5 mg/kg in avian species [1,33]. Four doses were tested: first dose, 1/20 of the toxic dose = 0.25 mg/kg; second dose, 1/10 of the toxic dose = 0.5 mg/kg; third dose, 1/5 of the toxic dose = 1 mg/kg; and fourth dose, 1/2.5 of the toxic dose = 2 mg/kg.…”

Effect of diclofenac on the pharmacokinetics of ciprofloxacin in quail

“…Diclofenac is a non-steroidal anti-inflammatory drug. The toxicokinetic in quail has belonged to metabolic capacity with t1/2 and mean residence time MRT above 8 hours with apparent signs of toxicities (2)(3)(4). Study of pharmacokinetics for enrofloxacin and ciprofloxacin in cow and steers showed the plasma elimination half-life for two drugs were longer in steers lactating cow than in cow (5).…”

Review - Gout In Chicken

“…The liver function markers AST and ALT were significantly increased in the birds effected with gout induced by high protein diet (Hong F et al, 2020) and diclofenac (Sandhyarani et al, 2019) which is an indication of hepatic injury. Antioxidant profile reveals decreased glutathione stimulating hormone (GSH) and increased thiobarbituric acid reactive substances (TBARS) in kidney and liver tissue (Singh et al, 2013;Akter and sarker, 2015;Sandhyarani et al, 2019). Glutathione (GSH) is an important intracellular peptide with multiple functions ranging from…”

“…Microscopically, marked congestion, hameorrhages involving glomeruli, cortical and medullary tubules, collecting ducts and medullary tracts and focal to diffuse degenerative changes in tubular epithelium like vacuolar degeneration, desquamated and necrosed tubular epithelial cells. Kidney parenchyma exhibited aggregates of uric acid crystals characterized by needle shaped urate crystals as pink radiating amorphous material surrounded by a narrow zone of inflammatory cells (Muhammed et al, 2012;Bulbule et al, 2013;Akter and sarker, 2015). Chandra and Balwant (1980) described the extent of damages to kidney was directly correlated to the degree of urate deposition.…”

“…Liver is enlarged, friable with white chalky urate deposition on the surface of the capsule. Liver section reveals severe sinusoidal congestion, haemorrhages in parenchyma, fatty change and foci of necrotic hepatocytes Sultana et al, 2012;Patel et al, 2014;Nitin and Ghosh, 2014;Amaravathi et al, 2015;Akter and sarker, 2015;Behtari and Feizi, 2015;Ramzan et al, 2015). Liver parenchyma shows amorphous radiating uric acid crystals mixed with necrotic debris surrounded by a narrow zone of inflammatory cells (Mudasir et al, 2017;Sandhyarani et al, 2019).…”