Early and Delayed Induction of DSBs by Nontargeted Effects in ICR Mouse Lymphocytes afterIn VivoX Irradiation

2016 ◽  
Vol 186 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Mitsuaki Ojima ◽  
Keiko Iwashita ◽  
Genro Kashino ◽  
Shinko Kobashigawa ◽  
Noriko Sasano ◽  
...  
Keyword(s):  
2008 ◽  
Vol 4 (1) ◽  
pp. 58-63
Author(s):  
Bin Na Hong ◽  
Tae Guy Park ◽  
Ha Na Hong ◽  
Tong Ho Kang

1990 ◽  
Vol 32 (5) ◽  
pp. 502-507 ◽  
Author(s):  
Tohru Sonoda ◽  
Shozo Ohdo ◽  
Ken-ichi Ohba ◽  
Takahiro Okishima ◽  
Kunio Hayakawa

2014 ◽  
Vol 7 (2) ◽  
pp. 111-115 ◽  
Author(s):  
Juliana Ivanova ◽  
Yordanka Gluhcheva ◽  
Sonja Arpadjan ◽  
Mariana Mitewa

ABSTRACT Cadmium (Cd) is a well-known nephrotoxic agent. Cd-induced renal dysfunction has been considered as one of the causes leading to the development of hypertension. The correlation between Cd concentration in blood and urine and cardiovascular diseases has been discussed in many epidemiological studies. A therapy with chelating agents is utilized for the treatment of toxic metal intoxication. Herein we present novel information indicating that monensin (applied as tetraethylammonium salt) is a promising chelating agent for the treatment of Cd-induced renal and cardiac dysfunction. The study was performed using the ICR mouse model. Adult ICR male mice were divided into three groups with six animals in each group: control (received distilled water and food ad libitum for 28 days); Cd-intoxicated (treated orally with 20 mg/kg b.w. Cd(II) acetate from day 1 to day 14 of the experimental protocol), and monensin treated group (intoxicated with Cd(II) acetate as described for the Cd-intoxicated group followed by oral treatment with 16 mg/kg b.w. tetraethylammonium salt of monensic acid for 2 weeks). Cd intoxication of the animals resulted in an increase of the organ weight/body weight indexes. Cd elevated significantly creatinine and glucose level in serum. Monensin treatment improved the organ weight/body weight ratios. The therapy of the Cd-intoxicated animals with monensin ameliorated the creatinine and glucose level in serum and decreased the concentration of the toxic metal ions in the heart and kidneys by 54 % and 64 %, respectively


2012 ◽  
Vol 26 (4) ◽  
pp. 279-284 ◽  
Author(s):  
Juliana Ivanova ◽  
Yordanka G. Gluhcheva ◽  
Kalina Kamenova ◽  
Sonja Arpadjan ◽  
Mariana Mitewa

1974 ◽  
Vol 140 (3) ◽  
pp. 779-796 ◽  
Author(s):  
Howard B. Dickler ◽  
David H. Sachs

Immunoglobulin complexes, composed of heat-aggregated human Ig, were shown to bind to mouse B lymphocytes of a variety of strains, but not to either thymocytes or thymus-derived (T) lymphocytes under a variety of conditions. It was shown that this binding was not due to either natural human antibodies against mouse nor to nonspecific binding of human Ig by mouse lymphocytes. Such complexes were shown to bind to the same sites which bind mouse antibody-antigen complexes. This site is known as the Fc receptor. The binding of Ig complexes to mouse B lymphocytes was markedly inhibited by pretreatment of the lymphocytes with anti-H-2 antisera. A series of experiments indicated the specificity of this result, including the fact that this inhibition was shown not to be due to the artifact of shedding of H-2 antibody-antigen complexes, nor to nonspecific steric inhibition. The antibodies within anti-H-2 antisera which were responsible for this inhibition were specific for alloantigens associated with the Ir region of the H-2 complex (Ia antigens). Antiserum specific for these Ia antigens produced inhibition, whereas antisera specific for antigens determined by the K or D regions of the H-2 complex did not. Evidence was obtained using F1 hybrid cells that at least some Ia antigens of both parental types are expressed on every B lymphocyte (i.e. codominant expression). These data indicate that the Fc receptor and a series of alloantigens controlled by the Ir region of the H-2 complex are identical or closely associated on the B-lymphocyte surface membrane. This observation may have implications for the mechanism of control of the immune response.


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