Oxidative Stress Induced by Diclofenac Alone and under the Influence of Certain Variables in Broilers


  • College of Veterinary Science, Rajendranagar, Departments of Pharmacology and Toxicology, Hyderabad, 500 030, India
  • College of Veterinary Science, Rajendranagar, Veterinary Pathology, Hyderabad, 500 030, India


Diclofenac toxicity was studied in male broiler chicks (Cobb strain) of a day old age. The chicks were randomly divided into eight groups consisting of 10 in each group. Group 1 was kept as basal diet control (1–32 days), group 2 on basal diet for 32 days + diclofenac (0.8 mg/kg body weight I/M) on day 24, 26, 28, 30, and 32, group 3 on basal diet for 32 days + cyclophosphamide (50 mg/kg body weight I/M once daily) from day 20 to 23, group 4 on high-protein, high-calcium, low vitamin A (HPHC) diet (1–32 days), group 5 on basal diet + diclofenac + cyclophosphamide (as per the schedule), group 6 on HPHC + diclofenac (as per the schedule), group 7 on HPHC + cyclophosphamide (as per the schedule), and group 8 on HPHC + diclofenac + cyclophosphamide (as per the schedule). The activity of TBARS, SOD, and catalase revealed a significant (P <0.05) increase, while there was a significant (P < 0.05) decrease in the concentration of GSH in liver in the groups given diclofenac either alone or in combination with other variables. There was no significant difference in the diclofenac residue levels. The electron microscopy of liver revealed lesions of mild to marked severity in different combinations. It can be concluded that diclofenac has the toxic potential in poultry at subtherapeutic doses and further the toxic effects were more pronounced under the influence of immunosuppressants and HPHC diet.


Diclofenac, hepatotoxicity, high-protein high-calcium diet, oxidative stress

Subject Discipline


Full Text:


Swan GE, Naidoo V, Richard C, Rhys EG, Deborah JP, Swarup D, et al. Removing the threat of diclofenac to critically endangered Asian Vultures. PLOS Biol 2006b;4:1-8.

Bird Life International. Threatened Birds of Asia: The Bird Life International Red Data Book. Cambridge UK: Bird Life International; 2001.

Gilbert M, Virani MZ, Watson RT, Oaks JL, Benson PC, Khan AA, et al. Breeding and mortality of Oriental White-backed Vulture Gyps bengalensis in Punjab Province, Pakistan Bird Conservation Intl 2002;12:311-26.

Oaks JL, Gilbertg M, Virani MZ, Watson RT, Meteyer CU, Rideout BA, et al. Diclofenac residues as the cause of vulture population decline in Pakistan. Nature 2004;427:630-3.

Subramanian KA, Manohar M, Mathan VI. An unidentified inhibitor of lipid peroxidation in intestinal mucosa. Biochem Biophysics Acta 1988;962:51-8.

Caliborne AL. Assay of catalase In: Greenwald RA, editor. Hand book of oxygen Radical Research. Baco-Raton: CRC press; 1985.

Moron MS, Depierre JW, Mannervik B. Levels of glutathione, glutathione reductase and glutathione-S-transferase in rat lung and liver. Biochem Biophysica Acta 1979;582:67-8.

Marklund S, Marklund G. Involvement of the superoxide Anion radical in the autooxidation of pyrogallol and a convenient assay for superoxide dismutase. European J Biochem 1974; 47:469-74.

Swan GE, Cuthbert R, Queredo M, Green RE, Deborah JP, Bartels P, et al. Toxicity of diclofenac to Gyps vultures. Biol Lett 2006a;2:279-82.

Hickey EJ, Raje RR, Reid VE, Gross SM, Ray SD. Diclofenac induced in vivo nephrotoxicity may involve oxidative stress mediated massive genomic DNA fragmentation and apoptotic cell death. Free Radical Biol Med 2001;31:139-52.

Sokol RJ, Straka MS, Daha R, Devereaux MW, Yerushalmi B, Gumpricht E, et al. Role of oxidant stress in the permeability transition induced in rat hepatic mitochondria by hydrophobic bile acid. Pediatric Res 2001;49:519-31.

Ponsoda X, Bort R, Jover R, Gomez Lechon MJ, Castell V. Molecular mechanism of diclofenac hepatotoxicity association of cell. Toxicol In Vitro 1995;7:439-44.

Gómez-Lechón MJ, Ponsoda X, O’Connor E, Donato T, Jover R, Castell JV. Diclofenac induces apoptosis in hepatocytes. Toxicol In Vitro 2003;17:75-80.

Boelsterli UA. Diclofenac-induced liver injury: A paradigm of idiosyncratic drug toxicity. Toxicol. Applied Pharmacol 2003;192:307-22.

Lim MS, Priscilla LK, Lin Gupta, Boetstrali UA. Critical role of free cytosolic calcium, but not uncoupling in mitochondrial permeability transition and cell death induced by diclofenac oxidative metabolites in immortalized human hepatocytes. Toxicol Applied Pharmacol 2006;217:322-31.


  • There are currently no refbacks.