TY - JOUR
T1 - Lead exposure causes thyroid abnormalities in diabetic rats
AU - Zadjali, Salah Al
AU - Nemmar, Abderrahim
AU - Fahim, Mohamed Abdelmonem Ay
AU - Azimullah, Sheikh
AU - Subramanian, Dhanasekaran
AU - Yasin, Javed
AU - Amir, Naheed
AU - Hasan, Mohammed Yousif
AU - Adem, Abdu
N1 - Publisher Copyright:
© 2015, E-Century Publishing Corporation. All rights reserved.
PY - 2015/5/30
Y1 - 2015/5/30
N2 - Lead is a widely-spread environmental pollutant and a commonly-used industrial chemical that can cause multisystemic adverse health effects. However, the effects of lead exposure on diabetic animals have not been reported so far. The aim of this study is to evaluate the effects of lead exposure on thyroid, renal and oxidative stress markers in diabetic Wistar rats. Diabetes was induced with an intraperitoneal (i.p.) injection of streptozocin (STZ). Six weeks later, rats were exposed i.p. to either distilled water (control group) or 25, 50 and 100 mg/kg of lead acetate (treatment groups). We found a positive relationship between the administered doses of lead acetate and its measured levels in blood samples (P < 0.01). Treatment of diabetic animals with lead acetate resulted in significant weight loss (P < 0.001). It also caused an increase in thyroid stimulating hormone levels (P < 0.05) and reductions in thyroxine (P < 0.05) and triiodothyronine levels (P < 0.01), a clinical picture consistent with hypothyroidism. Lead acetate exposure increased urea levels (P < 0.05) and caused a significant decrease in creatinine (P < 0.05). Besides, while the concentrations of malondialdehyde were not affected, glutathione stores were depleted (P < 0.01); in response to lead exposure. In conclusion, exposure of diabetic rats to lead acetate resulted in weight loss, clinical hypothyroidism, renal damage and oxidative stress.
AB - Lead is a widely-spread environmental pollutant and a commonly-used industrial chemical that can cause multisystemic adverse health effects. However, the effects of lead exposure on diabetic animals have not been reported so far. The aim of this study is to evaluate the effects of lead exposure on thyroid, renal and oxidative stress markers in diabetic Wistar rats. Diabetes was induced with an intraperitoneal (i.p.) injection of streptozocin (STZ). Six weeks later, rats were exposed i.p. to either distilled water (control group) or 25, 50 and 100 mg/kg of lead acetate (treatment groups). We found a positive relationship between the administered doses of lead acetate and its measured levels in blood samples (P < 0.01). Treatment of diabetic animals with lead acetate resulted in significant weight loss (P < 0.001). It also caused an increase in thyroid stimulating hormone levels (P < 0.05) and reductions in thyroxine (P < 0.05) and triiodothyronine levels (P < 0.01), a clinical picture consistent with hypothyroidism. Lead acetate exposure increased urea levels (P < 0.05) and caused a significant decrease in creatinine (P < 0.05). Besides, while the concentrations of malondialdehyde were not affected, glutathione stores were depleted (P < 0.01); in response to lead exposure. In conclusion, exposure of diabetic rats to lead acetate resulted in weight loss, clinical hypothyroidism, renal damage and oxidative stress.
KW - Diabetes
KW - Lead
KW - Rat
KW - Systemic toxicity
KW - Thyroid
UR - http://www.scopus.com/inward/record.url?scp=84937047059&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:84937047059
SN - 1940-5901
VL - 8
SP - 7160
EP - 7167
JO - International Journal of Clinical and Experimental Medicine
JF - International Journal of Clinical and Experimental Medicine
IS - 5
ER -