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Current IssueEditorial BoardOnline First ArticlesArchive

Research Article

volume 53 issue 9 (september 2019) : 1162-1166,   Doi: 10.18805/ijar.B-3633

Adverse effects of environmental lead exposure on hepatic, renal and thyroid function of buffaloes

S
Subrat Kumar Dash
S
Shashi Nayyar
S
Sandeep Sodhi Kakkar
R
Rajesh Jindal
1<div style="text-align: justify;">Department of Veterinary Physiology and Biochemistry, College of Veterinary Science, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana-141 004, Punjab, India.</div>
Cite article:- Dash Kumar Subrat, Nayyar Shashi, Kakkar Sodhi Sandeep, Jindal Rajesh (2019). Adverse effects of environmental lead exposure on hepatic, renal and thyroid function of buffaloes. Indian Journal of Animal Research. 53(9): 1162-1166. doi: 10.18805/ijar.B-3633.

ABSTRACT

Lead emitting industries pose a risk of contamination of surface and ground water, soil and fodder by dissemination of the particles carrying lead by wind action and by runoff from the tailings which cause numerous biochemical, immunological and reproductive disturbances in animals. Samples  (n-20) of tube-well water, surface soil and fodder were collected from an uncontaminated area with water lead level within the permissible limit (0.05µg/ml) which served as control, and from the lead contaminated area (n=25) of Ludhiana (Punjab) with water lead level above the permissible limit. Blood level of lead (>0.24µg/ml) was used to decide the exposure group. The biochemical profile of the buffaloes exposed to lead showed hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypertriglyridemia and hyperglycemia as compared to control group. The activity of serum enzymes viz alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase, alkaline phosphatase, lactate dehydrogenase and creatine kinase  showed significant (p<0.05) elevation in lead exposed buffaloes. There was significant (p<0.05) increase in levels of plasma urea and creatinine, however, tri-iodothyrinine and thyroxine concentrations were significantly (p<0.05) declined in lead exposed buffaloes as compared to control animals. Blood lead levels were significantly correlated with alterations in different biochemical indices in lead exposed buffaloes indicating the adverse effect on hepatic, renal and thyroid function. 

REFERENCES

  1. Ait Hamadouche N, Mehdid A, Guellil H, Slimani M and Aoues A E K (2014). Positive effects of green tea (Camellia Sinensis) on hepatic dysfunction induced by lead acetate in male rat. International J. Drug Dev. Res. 6(2): 87-96.
  2. Allen S E, Grimshaw H M and Rowland A P (1986). Methods in Plant Ecology. Eds., Blackwell Scientific Publication, Oxford, London.
  3. Anonymous (WHO) (2005). Guidelines for Drinking Water Quality. 3rd ed. World Health Organization.
  4. Aslani M R, Heidarpour M, Najarnezhad V, Mostakavi M and Khorasani Y T (2012). Lead poisoning in cattle associated with batteries recycling: High lead levels in milk of non symptomatic exposed cattle. Iranian J. Veterinary Sci. Tech. 4(1): 47-52.
  5. Chattopadhyay S, Ghosh S, Debnath J, Ghosh D (2001). Protection of sodium arsenite-induced ovarian toxicity by coadministration of L-ascorbate (vitamin C) in mature Wistar strain rat. Arch. Environmental Contamination Toxicol. 41: 83-89.
  6. El-Nekeety A A, El-Kady A A, Soliman M S, Hassan N S and Abdei-Wahhab M A (2009). Protective effect of Aqualegia vulgaris (L.) against lead acetate-induced oxidative stress in rats. Food Chemical Toxicol. 47: 2209-2215.
  7. Flora G, Gupta D and Tiwari A (2012). Toxicity of lead: a review with recent updates. Interdisciplinary Toxicol. 5(2): 47-58.
  8. Kaltreider R C, Davis A M, Lriviere J P and Hamilton J W (2001). Arsenic alters the function of the glucocorticoid receptor as a transcription factor. Environ. Health Persp. 109: 245-51.
  9. Kaneko J J, Harvey J W and Bruss M L (1997). Clinical Biochemistry of Domestic Animals. 6thed. Elsevier Inc., Oxford, United Kingdom.
  10. Koenig G and Seneff S (2015). Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk. Disease Markers Volume 2015, Article ID 818570, 18 pages, http://dx.doi.org/10.1155/2015/818570.
  11. Lafuente A, Gonzalez-Carraced A, Romero A, Cabaleiro T and Esquifino A I (2005).Toxic effects of cadmium on the regulatory mechanisms of dopamine and serotonin on prolactin secretion in adult male rats. Toxicol. Letters 155: 87-96
  12. Mohajeri G, Norouzian M A, Mohseni M and Afzalzadeh A (2014). Changes in blood metals, hematology and hepatic enzyme activities in lactating cows reared in the vicinity of a lead-zinc smelter. Bull. Environ. Contam. Toxicol. 92: 693-97.
  13. Nishiyama S, Nakamura K and Ogawa M (1985). Effects of heavy metals on corticosteroid production in cultured rat adrenocortical cells. Toxicol. Appl. Pharm. 81: 174-176.
  14. Parizanganeh A, Hajisoltani P and Zamani A A (2010). Assessment of heavy metal pollution in surficial soils surrounding zinc industrial complex in Zanjan-Iran. Proceed. Environ. Sci. 2:162-166.
  15. Pavia-Hunior M A, Paier B, Noli M I, Hagmuller K and Zaninovich A A (1997). Evidence suggesting that cadmium induces a non-    thyroidal illness syndrome in rat. J. Endocrin. 154: 113-117.
  16. Prabu S M, Muthumani M and Shagirtha K (2012). Protective effect of Piper betle leaf extract against cadmium-induced oxidative stress and hepatic dysfunction in rats. Saudi J. Biol. Sci. 19: 229-239.
  17. Radostitis O M, Blood D C, Gay C C and Hinchcliff H E (2000). Veterinary Medicine. A text Book of Disease of Cattle, Sheep, Pigs, Goats and Horses.10th ed. W B Saunders, London.
  18. Rana S V S (2014). Perspectives in endocrine toxicity of heavy metals- a review. Biol. Trace Elem. Res. 160: 1-14.
  19. Singh B, Chandran V, Bhandhu H K, Mittal B R, Bhattacharya A, Jindal S K and Verma S. 2000. Impact of lead exposure on pituitary-    thyroid axis in humans. BioMetals 13: 187-92.
  20. Valko M, Morris H and Cronin M T D. (2005). Metals, toxicity and oxidative stress. Current Med. Chem. 12: 1161-1208.
  21. Vries W, Romkens P F A M and Schutze G (2007). Critical soil concentrations of cadmium, lead and mercury in view of health effects on humans and animals. Rev. Environ. Cont. Toxicol. 191: 91-130.
  22. Winski S L and Carter D E (1998). Arsenate toxicity in human erythrocytes: characterization of morphologic changes and determination of the mechanism of damage. J. Toxicol. Environ Health-A 53(5): 345-355. 
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Indian Journal of Animal Research
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    Research Article

    volume 53 issue 9 (september 2019) : 1162-1166,   Doi: 10.18805/ijar.B-3633

    Adverse effects of environmental lead exposure on hepatic, renal and thyroid function of buffaloes

    S
    Subrat Kumar Dash
    S
    Shashi Nayyar
    S
    Sandeep Sodhi Kakkar
    R
    Rajesh Jindal
    1<div style="text-align: justify;">Department of Veterinary Physiology and Biochemistry, College of Veterinary Science, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana-141 004, Punjab, India.</div>
    Cite article:- Dash Kumar Subrat, Nayyar Shashi, Kakkar Sodhi Sandeep, Jindal Rajesh (2019). Adverse effects of environmental lead exposure on hepatic, renal and thyroid function of buffaloes. Indian Journal of Animal Research. 53(9): 1162-1166. doi: 10.18805/ijar.B-3633.

    ABSTRACT

    Lead emitting industries pose a risk of contamination of surface and ground water, soil and fodder by dissemination of the particles carrying lead by wind action and by runoff from the tailings which cause numerous biochemical, immunological and reproductive disturbances in animals. Samples  (n-20) of tube-well water, surface soil and fodder were collected from an uncontaminated area with water lead level within the permissible limit (0.05µg/ml) which served as control, and from the lead contaminated area (n=25) of Ludhiana (Punjab) with water lead level above the permissible limit. Blood level of lead (>0.24µg/ml) was used to decide the exposure group. The biochemical profile of the buffaloes exposed to lead showed hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypertriglyridemia and hyperglycemia as compared to control group. The activity of serum enzymes viz alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase, alkaline phosphatase, lactate dehydrogenase and creatine kinase  showed significant (p<0.05) elevation in lead exposed buffaloes. There was significant (p<0.05) increase in levels of plasma urea and creatinine, however, tri-iodothyrinine and thyroxine concentrations were significantly (p<0.05) declined in lead exposed buffaloes as compared to control animals. Blood lead levels were significantly correlated with alterations in different biochemical indices in lead exposed buffaloes indicating the adverse effect on hepatic, renal and thyroid function. 

    REFERENCES

    1. Ait Hamadouche N, Mehdid A, Guellil H, Slimani M and Aoues A E K (2014). Positive effects of green tea (Camellia Sinensis) on hepatic dysfunction induced by lead acetate in male rat. International J. Drug Dev. Res. 6(2): 87-96.
    2. Allen S E, Grimshaw H M and Rowland A P (1986). Methods in Plant Ecology. Eds., Blackwell Scientific Publication, Oxford, London.
    3. Anonymous (WHO) (2005). Guidelines for Drinking Water Quality. 3rd ed. World Health Organization.
    4. Aslani M R, Heidarpour M, Najarnezhad V, Mostakavi M and Khorasani Y T (2012). Lead poisoning in cattle associated with batteries recycling: High lead levels in milk of non symptomatic exposed cattle. Iranian J. Veterinary Sci. Tech. 4(1): 47-52.
    5. Chattopadhyay S, Ghosh S, Debnath J, Ghosh D (2001). Protection of sodium arsenite-induced ovarian toxicity by coadministration of L-ascorbate (vitamin C) in mature Wistar strain rat. Arch. Environmental Contamination Toxicol. 41: 83-89.
    6. El-Nekeety A A, El-Kady A A, Soliman M S, Hassan N S and Abdei-Wahhab M A (2009). Protective effect of Aqualegia vulgaris (L.) against lead acetate-induced oxidative stress in rats. Food Chemical Toxicol. 47: 2209-2215.
    7. Flora G, Gupta D and Tiwari A (2012). Toxicity of lead: a review with recent updates. Interdisciplinary Toxicol. 5(2): 47-58.
    8. Kaltreider R C, Davis A M, Lriviere J P and Hamilton J W (2001). Arsenic alters the function of the glucocorticoid receptor as a transcription factor. Environ. Health Persp. 109: 245-51.
    9. Kaneko J J, Harvey J W and Bruss M L (1997). Clinical Biochemistry of Domestic Animals. 6thed. Elsevier Inc., Oxford, United Kingdom.
    10. Koenig G and Seneff S (2015). Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk. Disease Markers Volume 2015, Article ID 818570, 18 pages, http://dx.doi.org/10.1155/2015/818570.
    11. Lafuente A, Gonzalez-Carraced A, Romero A, Cabaleiro T and Esquifino A I (2005).Toxic effects of cadmium on the regulatory mechanisms of dopamine and serotonin on prolactin secretion in adult male rats. Toxicol. Letters 155: 87-96
    12. Mohajeri G, Norouzian M A, Mohseni M and Afzalzadeh A (2014). Changes in blood metals, hematology and hepatic enzyme activities in lactating cows reared in the vicinity of a lead-zinc smelter. Bull. Environ. Contam. Toxicol. 92: 693-97.
    13. Nishiyama S, Nakamura K and Ogawa M (1985). Effects of heavy metals on corticosteroid production in cultured rat adrenocortical cells. Toxicol. Appl. Pharm. 81: 174-176.
    14. Parizanganeh A, Hajisoltani P and Zamani A A (2010). Assessment of heavy metal pollution in surficial soils surrounding zinc industrial complex in Zanjan-Iran. Proceed. Environ. Sci. 2:162-166.
    15. Pavia-Hunior M A, Paier B, Noli M I, Hagmuller K and Zaninovich A A (1997). Evidence suggesting that cadmium induces a non-    thyroidal illness syndrome in rat. J. Endocrin. 154: 113-117.
    16. Prabu S M, Muthumani M and Shagirtha K (2012). Protective effect of Piper betle leaf extract against cadmium-induced oxidative stress and hepatic dysfunction in rats. Saudi J. Biol. Sci. 19: 229-239.
    17. Radostitis O M, Blood D C, Gay C C and Hinchcliff H E (2000). Veterinary Medicine. A text Book of Disease of Cattle, Sheep, Pigs, Goats and Horses.10th ed. W B Saunders, London.
    18. Rana S V S (2014). Perspectives in endocrine toxicity of heavy metals- a review. Biol. Trace Elem. Res. 160: 1-14.
    19. Singh B, Chandran V, Bhandhu H K, Mittal B R, Bhattacharya A, Jindal S K and Verma S. 2000. Impact of lead exposure on pituitary-    thyroid axis in humans. BioMetals 13: 187-92.
    20. Valko M, Morris H and Cronin M T D. (2005). Metals, toxicity and oxidative stress. Current Med. Chem. 12: 1161-1208.
    21. Vries W, Romkens P F A M and Schutze G (2007). Critical soil concentrations of cadmium, lead and mercury in view of health effects on humans and animals. Rev. Environ. Cont. Toxicol. 191: 91-130.
    22. Winski S L and Carter D E (1998). Arsenate toxicity in human erythrocytes: characterization of morphologic changes and determination of the mechanism of damage. J. Toxicol. Environ Health-A 53(5): 345-355. 
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