DNA damage, Bcl-2, Bax expression and ultrastructure change in spermatogenic cell of mice exposed to cadmium / 中华劳动卫生职业病杂志
Chinese Journal of Industrial Hygiene and Occupational Diseases
;
(12): 271-273, 2005.
Article
in Chinese
| WPRIM
| ID: wpr-285906
ABSTRACT
<p><b>OBJECTIVE</b>To study DNA damage, Bcl-2 and Bax expression, and ultrastructure change in spermatogenic cell of mice by cadmium exposure.</p><p><b>METHODS</b>Twenty-four male mice were divided into 4 groups 3 groups treated with cadmium chloride of 1, 5, 10 micromol x kg(-1) x d(-1) i.p. respectively for 5 days, and one normal saline control group. The DNA damage of spermatogenic cell by single-cell gel electrophoresis technology was detected. The expression positive rate of Bcl-2, Bax protein in spermatogenic cell by the immunohistochemical method was assayed, and the ultrastructural change of spermatogenic cell by the transmission electron microscope was observed.</p><p><b>RESULTS</b>DNA damage rates of of spermatogenic cell in 1, 5, 10 micromol/kg cadmium chloride groups were higher than that of normal group (P < 0.001). Bcl-2 protein expression positive rates were lower than that of normal group (P < 0.001). Bax protein positive expression rate in 5 micromol/kg group was higher than those in normal group, and 1, 10 micromol/kg groups. The ultrastructure of karyotis, karyotheca, mitochondria, endoplasmic reticulum in three treated groups had different degree of damage and the degree of ultrastructural change was increasing with rising concentration of cadmium.</p><p><b>CONCLUSION</b>Cadmium exposure will cause the DNA break, Bcl-2 and Bax protein abnormal expression and ultrastructural change in spermatogenic cell.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Spermatozoa
/
DNA Damage
/
Proto-Oncogene Proteins
/
Apoptosis
/
Cadmium Chloride
/
Proto-Oncogene Proteins c-bcl-2
/
Bcl-2-Associated X Protein
/
Toxicity
/
Metabolism
/
Mice, Inbred ICR
Limits:
Animals
Language:
Chinese
Journal:
Chinese Journal of Industrial Hygiene and Occupational Diseases
Year:
2005
Type:
Article
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