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The aim of the study was to evaluate serum beta 2-microglobulin (beta-2m) and neopterin (NPT) in in patients with giardiasis. Twenty-two patients with giardiasis were examined and compared with twelve healthy subjects as a control group. Serum beta-2m and NPT concentration were determined twice: at the moment of diagnosis of giardiasis and six months after antiparasitic treatment with metronidazole. It was shown that serum beta-2m concentration in patients with giardiasis was remarkably elevated. It decreased significantly, but six months after treatment it was still higher as compared to the control group. However, serum NPT before antiparasitic treatment was slightly lower than in the control group, but after elimination of Giardia an increase of NPT concentration above control values was observed. It is concluded that Giardia infection leads to long-lasting disturbances in the immunological status of the host and may influence macrophage function and downregulate their parasiticidal effects.
The present study investigated the effects of single (lx) administration and a 10-day treatment with chelidonine (50 and 100 mg/kg i.p.) or drug Ukrain (7 and 14 mg/kg i.p.) on the ß2-microglobulin concentration in the serum of acute or subacute lead-poisoned rats (30 mg/kg i.p.). Both acute and subacute lead-intoxication significantly enhanced ß2- microglobulin concentration in the rats serum in comparison to the control groups. In acute poisoning only chelidonine (100 mg/kg i.p.) significantly decreased ß2-microgIo- bulin concentration in the rat serum. In subacute lead intoxication, 10-day treatment with chelidonine (50 mg/kg i.p.) or Ukrain (14 mg/kg i.p.) significantly decreased ß2- microglobulin in the serum of rats. Both chelidonine as well as Ukrain decreased nefrotoxicity induced by lead acetate. These investigations are to be continued.
Mercury is present in nature as metallic mercury, inorganic and organic compounds. Mercury levels constantly increase in the human natural environment. A similar rise of mercury content has been observed in human tissues. Kidney disease arising from exposure to heavy metals, mainly during occupational exposure to mercury, may play a special role in nephrology. Long-term exposure to mercury may cause progressive degenerative changes in the kidneys, possibly leading to renal insufficiency. The main renal changes caused by mercury are indicated by the both glomerular and tubular disfunction. Early renal damage may usually be monitored by measurements in urine excretion of very sensitive small proteins and of some enzymes. This article reviews data concerning the nephrotoxic effects of mercury compounds in animals and humans induced by exposure to mercury compounds with the results of our study in changes of proteins in urine excretion in groups of workers occupationally exposed to mercury vapours, (depending on degree and duration of exposure).
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