Biochemical and genotoxic response of naphthalene to fingerlings of milkfish Chanos chanos.

L Palanikumar, A K Kumaraguru, C M Ramakritinan
Author Information
  1. L Palanikumar: Department of Marine and Coastal Studies, School of Energy, Environment and Natural Resources, Madurai Kamaraj University, Madurai, 625021, India. palanikumarl@gmail.com

Abstract

The present study investigated the acute toxicity, sub-lethal toxicity and biochemical response of naphthalene in fingerlings of milkfish Chanos chanos. The 96 h acute toxicity LC50 values for C. chanos exposed to naphthalene was 5.18 μg l(-1). The estimated no observed effect concentration and lowest observed effect concentration values for naphthalene in C. chanos were 0.42 and 0.69 μg l(-1) respectively for 30 days. The estimated maximum allowable toxicant concentration for naphthalene was 0.53 μg l(-1). Biochemical enzyme markers such as lipid peroxidation, catalase, glutathione S transferase and reduced glutathione were measured in gills and liver tissues of C. chanos exposed to sub-lethal concentrations of naphthalene. Fluctuation in lipid peroxidation and catalase level suggests that naphthalene concentrations play a vital role in induction of oxidative stress in fish. Induction of reduced glutathione level and inhibition of glutathione S-transferase level was observed in naphthalene exposed C. chanos suggesting that there may be enhanced oxidative damage due to free radicals. Increasing concentration increases in number of nuclear abnormalities. The formation of micronuclei and binucleated micronuclei induction by naphthalene confirm its genotoxic potential. The highest levels of DNA damage (% tail length) were observed at 1.24 μg l(-1) of naphthalene. The study suggests that biochemical enzymes, nuclear abnormalities and DNA damage index can serve as a biological marker for naphthalene contamination.

References

  1. Mar Pollut Bull. 2004 Mar;48(5-6):429-33 [PMID: 14980458]
  2. Ecotoxicol Environ Saf. 2002 Feb;51(2):115-27 [PMID: 11886185]
  3. Mutat Res. 2003 Jan 10;534(1-2):65-75 [PMID: 12504755]
  4. Bull Environ Contam Toxicol. 1996 Mar;56(3):425-31 [PMID: 8825965]
  5. Environ Pollut. 2006 Jun;141(3):443-51 [PMID: 16271429]
  6. Aquat Toxicol. 2001 May;52(3-4):189-203 [PMID: 11239681]
  7. Mutat Res. 1994 May 1;307(1):261-71 [PMID: 7513806]
  8. Fish Physiol Biochem. 2009 Jun;35(2):293-9 [PMID: 19343524]
  9. Aquat Toxicol. 2011 Oct;105(3-4):300-11 [PMID: 21781655]
  10. J Biol Chem. 1974 Nov 25;249(22):7130-9 [PMID: 4436300]
  11. Ecotoxicol Environ Saf. 2010 Nov;73(8):1842-51 [PMID: 20843549]
  12. Biochem Pharmacol. 2003 Oct 15;66(8):1499-503 [PMID: 14555227]
  13. Methods Enzymol. 1978;52:302-10 [PMID: 672633]
  14. Ecotoxicol Environ Saf. 2002 Jul;52(3):180-9 [PMID: 12297077]
  15. Ecotoxicol Environ Saf. 2004 Mar;57(3):290-302 [PMID: 15041252]
  16. Environ Monit Assess. 2011 Nov;182(1-4):205-13 [PMID: 21213039]
  17. Sci Total Environ. 2008 Jun 1;395(2-3):87-100 [PMID: 18346779]
  18. Aquat Toxicol. 2012 Oct 15;122-123:1-8 [PMID: 22717255]
  19. Environ Sci Pollut Res Int. 2012 Mar;19(3):609-18 [PMID: 21881906]
  20. Mar Pollut Bull. 2001 Aug;42(8):656-66 [PMID: 11525283]
  21. Sci Total Environ. 2006 Dec 15;372(1):157-63 [PMID: 17078999]
  22. Environ Sci Pollut Res Int. 2010 Feb;17(2):441-52 [PMID: 19798526]
  23. Aquat Toxicol. 2006 Jan 5;76(1):69-92 [PMID: 16290221]
  24. Anal Biochem. 1976 Jul;74(1):214-26 [PMID: 962076]
  25. Mutat Res. 1997 Apr 24;390(1-2):33-44 [PMID: 9150750]
  26. Arch Environ Contam Toxicol. 1995 Jan;28(1):1-7 [PMID: 7717759]
  27. Ecotoxicol Environ Saf. 1999 Jan;42(1):67-74 [PMID: 9931241]
  28. Arch Environ Contam Toxicol. 1998 Jul;35(1):58-63 [PMID: 9601920]
  29. Bull Environ Contam Toxicol. 2013 Jan;90(1):60-8 [PMID: 23196369]
  30. Biomarkers. 2012 May;17(3):275-85 [PMID: 22435595]
  31. Ecotoxicol Environ Saf. 2012 Jan;75(1):187-97 [PMID: 21944957]
  32. Comp Biochem Physiol C Toxicol Pharmacol. 2005 Jan;140(1):115-21 [PMID: 15792630]
  33. Ecotoxicology. 2009 Jan;18(1):75-80 [PMID: 18763036]
  34. Chemosphere. 2009 Dec;77(11):1495-500 [PMID: 19880156]
  35. Exp Cell Res. 1988 Mar;175(1):184-91 [PMID: 3345800]
  36. Int J Toxicol. 2004;23(5):301-33 [PMID: 15513831]
  37. Ecotoxicol Environ Saf. 2006 Jun;64(2):178-89 [PMID: 16406578]
  38. Mutat Res. 1995 Oct;335(2):109-20 [PMID: 7477041]
  39. Physiol Rev. 2005 Jan;85(1):97-177 [PMID: 15618479]
  40. Ecotoxicol Environ Saf. 2001 May;49(1):64-75 [PMID: 11386717]
  41. Chemosphere. 2004 Apr;55(2):167-74 [PMID: 14761689]
  42. J Biol Chem. 1951 Nov;193(1):265-75 [PMID: 14907713]

MeSH Term

Animals
Catalase
Chemical Phenomena
Comet Assay
DNA Damage
Environmental Exposure
Fishes
Gills
Glutathione
Glutathione Transferase
Inhibitory Concentration 50
Lipid Peroxidation
Liver
Micronucleus Tests
Naphthalenes
Oxidative Stress
Toxicity Tests, Acute
Water Pollutants, Chemical

Chemicals

Naphthalenes
Water Pollutants, Chemical
naphthalene
Catalase
Glutathione Transferase
Glutathione

Word Cloud

Created with Highcharts 10.0.0naphthalenechanosCμgl-1observedconcentrationglutathionetoxicityexposed0leveldamagestudyacutesub-lethalbiochemicalresponsefingerlingsmilkfishChanosvaluesestimatedeffectBiochemicallipidperoxidationcatalasereducedconcentrationssuggestsinductionoxidativenuclearabnormalitiesmicronucleigenotoxicDNApresentinvestigated96hLC50518lowest4269respectively30daysmaximumallowabletoxicant53enzymemarkersStransferasemeasuredgillslivertissuesFluctuationplayvitalrolestressfishInductioninhibitionS-transferasesuggestingmayenhancedduefreeradicalsIncreasingincreasesnumberformationbinucleatedconfirmpotentialhighestlevels%taillength124enzymesindexcanservebiologicalmarkercontamination

Similar Articles

Cited By (6)