Toxic effects of prenatal Ipomoea carnea administration to rats.

Chronic exposure of livestock to Ipomoea carnea, a toxic plant, promotes toxicosis characterized by lysosomal vacuolization of different organs, and is clinically manifested by CNS signs, abnormal endocrine and gastrointestinal functions, alteration of the immune system, and abnormal embryogenesis. The present study evaluated the effects of different doses of the plant extract on pregnant rats and their offspring after oral administration to the dams from day 6 to day 20 of gestation. Histopathology of thyroid, pancreas, liver and kidneys of dams on gestational day 21 showed characteristic vacuolization promoted by I. carnea toxicosis in these organs; the same was observed in the organs of 7-d-old pups. On the other hand, no alteration was found in these same organs of dams the 7th d after parturition. Although the lesions were reversed in the dams, the same did not occur in their pups. I. carnea administration also promoted decreased body weight, thymus atrophy and spleen enlargement in pups. The toxic principle of I. carnea (swainsonine) seems to pass through the placenta.

Evaluation of immunomodulatory activity of Ipomoea carnea on peritoneal cells of rats.

In the present study, animals of the experimental groups were treated with an aqueous fraction (AF) of Ipomoea carnea diluted in drinking water in order to obtain daily doses of 3gdryleaves/kg/body weight (bw) and 15g/kg/bw for 14 and 21 days, or by gavage 15g/kg/bw administered for 14 days, respectively. Peritoneal macrophages were collected and submitted to the spreading, phagocytosis, and hydrogen peroxide release tests. AF administration in drinking water for 14 and 21 days promoted increased macrophage phagocytosis activity and hydrogen peroxide release. However, the administration of 15g/kg/bw of AF by gavage for 14 days resulted in no alteration in macrophage activity. These results suggest that low dosages of Ipomoea carnea induced enhanced phagocytosis activity and hydrogen peroxide production by macrophages.

Effects of high doses of diazepam on carrageenin-induced paw edema in rats.

Benzodiazepine (BDZ) receptor sites play a relevant role in immune/inflammatory reactions. Acute BDZ treatments were shown not only to suppress cell proliferation in rat thymus but also to decrease TNF-alpha, IL-1 and IL-6 release from adult mouse macrophages. In the present investigation the effects of acute (10.0 and 20.0 mg/kg) and long-term (10.0 mg kg-1 day-1, for 21 days) diazepam treatment on carrageenin-induced paw edema were studied in rats. The results showed that acute treatment with high doses of diazepam decreased paw edema volume in a dose-dependent manner, and this effect was observed as early as 1 h after the administration of the 20.0 mg/kg dose and continued until the last measurement was performed (8 h). In contrast, long-term diazepam administration did not modify the phlogistic-induced edema. Taken together, these data show that 1) acute diazepam treatment with high doses decreases the volume of the acute inflammatory paw edema developed by the organism as a response to carrageenin-induced injury, and 2) long-term diazepam treatment induces tolerance to this effect. These results are discussed in the light of a possible effect of diazepam on the components of the rat cellular and humoral immune/inflammatory reaction such as T lymphocytes and/or interleukins.

Effects of high doses of diazepam on carrageenin-induced paw edema in rats

Benzodiazepine (BDZ) receptor sites play a relevant role in immune/ inflammatory reactions. Acute BDZ treatments were shown not only to suppress cell proliferation in rat thymus but also to decrease TNF-alpha, IL-1 and IL-6 release from adult mouse macrophages. In the present investigation the effects of acute (l0.0 and 20.0 mg/kg) and long-term (10.0 mg kg(-1) day(-l), for 21 days) diazepam treatment on carrageenin-induced paw edema were studied in rats. The results showed that acute treatment with high doses of diazepam decreased paw edema volume in a dose-dependent manner, and this effect was observed as early as 1 h after the administration of the 20.0 mg/kg dose and continued until the last measurement was performed (8 h). In contrast, long-term diazepam administration did not modify the phlogistic-induced edema. Taken together, these data show that 1) acute diazepam treatment with high doses decreases the volume of the acute inflammatory paw edema developed by the organism as a response to carrageenininduced injury, and 2) long-term diazepam treatment induces tolerance to this effect. These results are discussed in the light of a possible effect of diazepam on the components of the rat cellular and humoral immune/inflammatory reaction such as T lymphocytes and/or interleukins.

Acute, subchronic and chronic 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication in rats.

The acute, subchronic and chronic toxicities of 2,4-dichlorophenoxyacetic acid (2,4-D) were studied ir rats. Animals were exposed acutely (600 mg/kg), subchronically (200 ppm for 30 d) and chronically (200 ppm for 180 d) to 2,4-D by the oral route. Clinical, laboratory and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased locomotor activity and induced ataxia, sedation, muscular weakness (mainly of the hind quarters) and gasping for breath; increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), amylase activities and creatinine levels; decreased total protein (TP) and glucose levels; and increased hematocrit values. Subchronic and chronic 2,4-D exposures did not induce overt clinical signs or symptoms of intoxication. However, subchronic herbicide exposure increased AST activity and albumin and hematocrit values, and chronic exposure increased AST, AP and LDH activities, decreased amylase and glucose levels, but did not change hematocrit values. Chromatographic analysis of the serum of chronically exposed rats showed the presence of the herbicide; the amount found (3.76 +/- 1.16 micrograms/ml) suggested the absence of 2,4-D accumulation within the body. Although macroscopic or histopathological lesions were not observed in acutely, subchronically or chronically 2,4-D exposed rats, the laboratory data obtained suggest tissue injuries after dosing, since the results are considered early indicators of primarily hepatic and muscle tissue damage.

Effects of acute 2,4-dichlorophenoxyacetic acid on cattle serum components and enzyme activities.

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D) was studied in cattle. Steers were dosed po with 100, 300 or 600 mg 2,4-D/kg bw. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), O-glutamyl transferase (O-GT), creatine kinase (CK), lactate dehydrogenase (LDH) activities and urea, creatinine, glucose, total proteins and albumin levels were determined at intervals after dosing. The lowest 2,4-D dose did not change the biochemical parameters studied; the 300 mg/kg dose decreased AST, O-GT and CK activities and increased urea and glucose levels; the highest dose of 2,4-D increased LDH and CK activities and protein, urea, creatinine and glucose levels. These changes were time and dose-dependent and completely reversible. Acute 2,4-D intoxication disrupted the serum levels of several enzymes and blood components which mainly reflect kidney and muscle damage induced by the herbicide.

Acute 2,4-dichlorophenoxyacetic acid intoxication in cattle.

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D) was studied in cattle. Steers were orally treated with 100, 300 or 600 mg 2,4-D/kg. Behavioral alterations, heart and respiratory functions, rectal temperature and ruminal movements were observed at 2, 4, 8, 12, 24, 48, 72 and 96 h after treatment. At these moments, blood and urine samples were collected and serum 2,4-D levels were determined. Results show that animals' vital function and hematocrit were not modified by the herbicide. Other signs were doses and time-dependent and included motor alterations (weakness, lethargy, decreased general activity) and decreased ruminal movements and proteinuria. The herbicide was rapidly excreted and the intoxication signs were completely reserved. 2,4-D is an herbicide of small toxicological consequences for cattle kept under in natural grazing systems.

Effects of acute 2,4-dichlorophenoxyacetic acid intoxication on some rat serum components and enzyme activities.

The present study was undertaken to investigate the effects of acute 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication (0.6 g/kg, po) on lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, amylase, creatinine, glucose, total protein and albumin levels in rats. Serum levels of lactate dehydrogenase, alkaline phosphatase and creatinine increased from 1- to 4-fold at 5, 8 and 24 h after 2,4-D administration, whereas serum levels of aspartate and alanine aminotransferase were higher only at 8 and 24 h. Amylase levels were only increased 8 h after administration of 2,4-D and then returned to normal levels. In contrast, 2,4-D reduced the serum levels of glucose and total protein 5, 8 and 24 h and serum albumin levels 5 h after herbicide intoxication. Thus, acute intoxication with 2,4-D disrupts serum levels of several enzymes and components which are considered to be indicators of tissue injury. Most likely these alterations mainly reflect hepatic and muscle tissue damage induced by the herbicide, but significant pancreatic and kidney toxicity may also have occurred.

Effects of acute 2,4-dichlorophenoxyacetic acid intoxication on some rat serum components and enzyme activities

The present study was undertaken to investigate the effects of acute 2,4-dichlorophenoxacetic acid (2,4-D) intoxication (0.6 g/kg, po) on lactate dehydrogenase, alkaline phosphatase, aspartate amino-transferase, alanine aminotransferase, amylase, creatinine, glucose, total protein and albumin levels in rats. Serum levels of lactate dehydrogenase, alkaline phosphatase and creatinine increased from 1-to 4-fold at 5,8 and 24 h after 2,4-D administration, whereas serum levels of aspartate and alanine aminotransferase were higher only at 8 and 24 h. Amylase levels were only increased 8 h after administration of 2,4-D and then returned to normal levels. In contrast, 2,4-D reduced the serum levels of glucose and total protein 5,8 and 24 h and serum albumin levels 5 h after herbicide intoxication. Thus, acute intoxication with 2,4-D disrupts serum levels of several enzymes and components which are considered to be indicators of tissue injury. Most likely these alterations mainly reflect hepatic and muscle tissue damage induced by the herbicide, but significant pancreatic and kidney toxicity may also have occurred