Cadmium (Cd) is a widely distributed environmental pollutant. It is found in the air, water and soil, which makes significant hazard to human organism. Given the long-term income inhalation Cadmium harmful effect on the respiratory system, affecting lungs, where accumulated significant proportion of Cd2+ from contaminated air. This element causes the development of chronic obstructive pulmonary disease, fibrosis, emphysema and cancer-causing effect. It is established that the introduction of cadmium intraperitoneal as injection (0.5–2.0 mg / kg) to animals leads to separation of the cells of inflammatory cytokines (TNF, IL-6), development of inflammatory response and lung infiltration of neutrophils. It is believed that due to the evolution of proteinase activated white blood cells is a major damaging factor in the development of respiratory lesions cations Cd2+.

Environmental exposure to this pollutant, contamination of foods and forages with cadmium and other heavy metals has become a source of human and animal illness worldwide.

Therefore the study of mechanisms of cadmium action on living organisms is an important issue for contemporary biochemistry and ecology. During recent years many experiments have been carried out in order to study the effects of cadmium on liver, kidney, lung, central nervous system. But effects of this metal on the immune system and metabolism in leukocytes of peripheral blood have not been investigated well. It especially concerns the long-time influence of low doses of heavy metal on animal organism. The aim of present research was to study the effects of cadmium chloride long time intake in low doses several processes of metabolism in neutrophilic granulocytes of the rat.

The investigations of metabolic effects of cadmium after the long-time period have shown the changes in enzyme of energy metabolism activities in neutrophilic granulocytes of rats. For instance, after 21-day period of heavy metal administration pyruvate kinase activity was reduced throughout the experiment, indicating significant changes of anaerobic metabolism in neutrophilic granulocytes.

However, the activity of the enzyme that catalyzes the step of glycolysis – lactate dehydrogenase – decreased on the 14th day of administration of toxicants in neutrophilic granulocytes and increased in the final stages of research. Analyzing glucose-6-phosphate dehydrogenase activity of neutrophilic granulocytes should be noted that enzyme activity gradually decreased during the experiment, the most expressive change was observed on the 21st day of administration of cadmium chloride. Inhibition of glucose-6-phosphate dehydrogenase activity in neutrophilic granulocytes negatively affect to antimicrobial and antioxidant action because of inhibition of the recovery process NADP necessary for the functioning of NADPH-oxidase. This applies particularly to the final stage of research (on the 21st day of cadmium chloride administration). The results of investigations show the reorganization of some metabolic processes of energy metabolism in the neutrophilic granulocytes under the influence of cadmium.

Thus, lactate dehydrogenase activities were increased in leukocytes of the rats, which were influenced with cadmium chloride, but inhibition pyruvate kinase and glucose- 6-phosphate dehydrogenase in neutrophilic granulocytes an the end of the investigation may cause significant decrease in the ability of these cells to phagocytosis and bactericidal action, and therefore their functional activity gradually suppressed with the duration of administration of cations Cd2+.

Keywords: cadmium chloride, energy metabolism, neutrophylic granulocytes, immune system

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1. 1. Astaurov B. Methods biology development .1974.346-433.
2. 2. Dmytrukhа N.Тhe question nephrotoxic action Cadmiu. Ukrainian Journal of the problems of Occupational Medicine. 2010;2(22):36-42.
3. 3. Boyum A.Оne- stage procedure for isolation of granulocytes and lymphocytes from human blood. Scand.: J. Clin. Lab. Invest; 1968. 21.
4. 4. Bedard K,Krause K. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.Physiol. Rev. 2007;87(1):245-313.
5. 5. Beyersmann D,Hechtenberg S. Cadmium, gene regulation, and cellular signalling in mammalian cells.Toxicol. Appl. Pharmacol. 1997;144(2):247-261.
6. 6. Krishnamurthy V, Gunalan G, Haridas S, Thangamani V.Biochemical changes in neutrophilsof cervical cancer patients treatedwith 60Co.Current Sci. 2008;94(9):1995-1999.
7. 7. Cannino G, Ferruggia E, Luparello C, Rinaldi A.Cadmium and mitochondria.Mitochondrion. 2009;9(6):377-384. doi.org/10.1016/j.mito.2009.08.009
8. 8. Ozlü F, Satar M, Menziletoğlu-Ylldlz S, Unlükurt I, Aksoy K.Glucose-6-phosphate dehydrogenase activity, structure, molecular characteristics and role in neonatal hyperbilirubinemia in cord blood in Cukurova region.Turk. J. Pediatr. 2011;53(2):130-136.
9. 9. Satarug S, Garrett S, Sens M, Sens D.Cadmium, environmental exposure, and health outcomes. Environ. Health Perspect. 2010;118(2):182-190. doi.org/10.1289/ehp.0901234
10. 10. Joseph P. Mechanisms of cadmium carcinogenesis.Toxicol. Appl. Pharmacol. 2009;238(3):272-279.
11. 11. Lippolis J. Immunological signaling networks: Integrating the body's immune response.J. Anim. Sci. 2008;86(14):E53-E63.
12. 12. Massadeh A,Al-Safi S.Analysis of cadmium and lead: their immunosuppressive effects and distribution in various organs of mice.Biol. Trace Elem. Res. 2005;108(1-3):279-286.
13. 13. Sokolova I. Cadmium effects on mitochondrial function are enhanced by elevated temperatures in a marine poikilotherm, Crassostrea virginica Gmelin (Bivalvia: Ostreidae).J. Exp. Biol. 2004;207(15):2639-2648.
14. 14. Thévenod F. Cadmium and cellular signaling cascades: to be or not to be?Toxicol. Appl. Pharmacol. 2009;238(3):221-239.
15. 15. Wirth J,MijalR. Adverse effects of low level heavy metal exposure on male reproductive function.Syst. Biol. Reprod. Med. 2010;56(2):147-167.
16. 16. Van Den Heuvel R,LeppensH, SchoetersG. Useofinvitroassaystoassesshematotoxiceffectsofenvironmentalcompounds.CellBiol.Toxicol. 2001;17(2):107-116.
17. 17. Yu B. Cellular defences against damage from reactive oxygen species. Physiol. Rev. 1994;74(1):139-162.