Chronic exposure of adult rats to dietary untake of cadmium (15 mg CdCl2/day/kg for 30 days) leads to development of anemia and thrombocytosis. Anemia is characterized by significant reticulocytosis (13.1 ± 1.0%), anysocytosis, poikilocytosis, iron deficiency and marked alterations of antioxidant and metabolic status of red blood cells. Activities of SOD, catalase, GPx and GR were significantly increased in red blood cells of cadmium‐treated rats. In treated animals cadmium induced an increase of red cell reduced and oxidized glutathione with no changes of GSSG/GSH ratio. However, significant reduction of lipid peroxidation was found. Plasma levels of tocopherol and ascorbate, as well as activity of glutathione‐S‐transferase, were all significantly increased in cadmium‐treated rats. The energy metabolism of red blood cells was deeply altered in cadmium‐treated rats. The levels of ATP, ADP, AMP and TAN were significantly increased while ATP/ADP ratio and adenylate energy charge (AEC) were significantly reduced. The level of 2,3‐BPG was somewhat lower, but 2,3‐BPG/Hb ratio was considerably higher, in red blood cells of cadmium‐treated rats.

We found greater renal, hepatic, and LA RI in patients with liver cirrhosis than in healthy controls. The correlation we found between elevated renal artery RI (≥0.70) and MELD score emphasizes the risk of renal dysfunction during progression of liver cirrhosis.

In this paper, first, we consider the existence of a positive solution for the nonlinear fractional differential equation boundary value problem CnormalDαu(t)+f(t,u(t))=0,1em0

induced values of MN and CBPI, so that absence of T1 and M1 isoenzymes did not cause increased mutagen sensitivity of PBLs of DTC patients.