Biochemical and histopathological parameters of the hepatic function were used to quantify the hepatotoxic effects of atrazine in female pigs (gilts) undergoing intensive breeding. Female pigs (cross-bred Swedish and German landrace) received 2 mg atrazine kg-1 body wt. in feed daily during 19 days of the oestrous cycle. The last treatment day corresponded to day -3 of the onset of the next expected oestrus. Blood samples were collected three times daily at 3-h intervals on the first four post-treatment days. Serum activities of gamma-glutamyltransferase (GGT), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (AP) were determined. Serum activity of GGT was significantly increased throughout the four post-treatment days. In comparison with the control values, a slight but not significant decrease was observed in the serum activities of ALT, AST and AP. Histopathological examination of the liver of exposed pigs showed mild centrolobular parenchymatous degeneration. Interstitial connective tissue proliferation resulted in narrow and irregular bile canaliculi.
The aim of the study was to evaluate the effect of adrenal stimulation by adrenocorticotropic hormone (ACTH) on blood cortisol concentration and on circulating total and differential leukocyte counts during and in the 16 days after ACTH administration. Swedish Landrace boars aged approximately 6-7 months were used. ACTH-treated animals (n = 7) were given ACTH intravenously at 10 microg/kg body mass for 3 days. A control group of animals (n = 7) received 1 ml of sterile 0.9% saline intramuscularly. ACTH induced a highly significant increase (p>0.0001) in serum cortisol in treated boars. On the day after the last ACTH dose, the cortisol concentration was significantly higher, but the level of significance was lower than during ACTH administration (p>0.05). During ACTH treatment, a significant increase was recorded in total leukocyte count and neutrophil percentage (p>0.05 to p>0.0001), along with the increase in blood cortisol concentration, whereas percentage lymphocyte count showed a significant decrease. Lymphopenia disappeared upon cessation of treatment, but neutropenia developed in the week after treatment. On all three days of ACTH challenge, the neutrophil-to-lymphocyte ratio was significantly increased. An increase in eosinophil percentage was recorded on treatment days 1 and 2, whereas ACTH treatment had no effect on basophil percentage. In conclusion, three-day administration of ACTH to young boars during restraint caused effects similar to acute stress situations, as suggested by disappearance of the effects on immune function after the last drug dosage.
The effects of stress induced by adrenocorticotropic hormone (ACTH) on biochemical and immune changes in Swedish Landrace boars aged approximately 6-7 months were observed during ACTH administration and for 16 days after the cessation of treatment. Adrenocorticotropic hormone treated animals (n = 7) were given intravenously 10 microg/kg body mass of ACTH for 3 days. Control group of animals (n = 7) received intramuscularly 1 ml of sterile 0.9% saline. Total protein and globulin levels were significantly elevated during the induced stress period and for the next 16 days (P < 0.01 to P < 0.0001, respectively). Also, serum immunoglobulin IgG concentration was significantly elevated during and after ACTH injection (P < 0.001 to P < 0.0001). Adrenocorticotropic hormone treatment had no effect on serum albumin, IgA and IgM concentrations. Glucose concentration was significantly decreased on the second day of ACTH administration (P < 0.001) and on day 9 after treatment (P < 0.001). Calcium level was significantly decreased only for 24 h after the last ACTH dosage (P < 0.01). Also, serum phosphorus level was significantly decreased on the first (P < 0.05) and third (P < 0.001) days of ACTH challenge but remained unaffected after the cessation of ACTH treatment. It is concluded that the administration of ACTH to boars results in immune humoral and biochemical changes during stress and the post-stress period.
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