Influence of urea-calcium mixtures as rumen slow-release feed on in vitro fermentation using a gas production technique

In this experiment the effects of different urea products (urea [U] and urea-calcium mixtures [UCM]) on rumen fermentation were investigated in dependence of different energy sources by using in vitro techniques. The 7 x 2 factorial arrangement followed a completely randomised design using seven urea products (U100, U40CaCl2, U50CaCl2, U60CaCl2, U40CaSO4, U50CaSO4 and U60CaSO4) in combination with cassava chips (CC) or corn meal (CM). Compared with other treatments, the cumulative gas production (96 h) was significantly increased for U60CaCl2 + CC and U60CaSO4 + CC (p < 0.01), which was combined with a higher in vitro true digestibility (p < 0.01). In addition, the concentration of volatile fatty acids in the fluid of U60CaCl2 + CC and U60CaSO4 + CC was significantly higher than in other treatments. Urea treatments (U100 + CC and U100 + CM) caused the highest concentration of ruminal ammonia nitrogen (p < 0.01), which was significantly decreased by all UCM products in combination with CC, but not with CM. The highest levels of total bacteria, Fibrobacter succinogenes and anaerobic fungi were found for treatment U60CaCl2 + CC and U60CaSO4 + CC (p < 0.05). The findings revealed that the utilisation of U60CaCl2 and U60CaSO4 in combination with cassava chips improved the ruminal fluid fermentation in terms of NH3-N and volatile fatty acid concentration, digestibility of energy and increased the fibrobacter concentrations.     

Erythrocyte pyrimidine 5'-nucleotidase inhibition by acute lead exposure in neonatal rats

Inhibition by lead of erythrocyte pyrimidine 5'-nucleotidase (P5N) is thought to contribute to morphological abnormalities observed in red blood cells (RBC) of lead-exposed subjects. However, neither the mechanism of lead inhibition of P5N nor the relationship of this inhibition to blood lead levels attained in exposed subjects is known. In the present investigation, acute in vivo and in vitro lead acetate effects on erythrocyte P5N from 21-day-old rat pups were determined and were related to blood lead concentrations ascertained by atomic absorption spectrophotometry. Acute lead administration to rat pups resulted in a 16% to 21% reduction in erythrocyte P5N, with mean blood lead levels ranging from 77 to 108 micrograms/dl 24 hours later. Inhibition of erythrocyte P5N was linearly related to blood lead level (r = -0.67, P less than 0.05) following acute lead administration. Lead acetate addition to RBC preparations from 21-day-old rats resulted in concentration-dependent P5N inhibition which was comparable to that produced following acute in vivo exposure. The results indicate that acute P5N inhibition in lead-treated neonatal rats is due to noncompetitive P5N inhibition by lead. The inhibition of P5N produced by acute lead treatment is linearly related to blood lead concentrations.     

Erythrocyte pyrimidine 5′-nucleotidase inhibition by acute lead exposure in neonatal rats

Inhibition by lead of erythrocyte pyrimidine 5′-nucleotidase (P5N) is thought to contribute to morphological abnormalities observed in red blood cells (RBC) of lead-exposed subjects. However, neither the mechanism of lead inhibition of P5N nor the relationship of this inhibition to blood lead levels attained in exposed subjects is known. In the present investigation, acute in vivo and in vitro lead acetate effects on erythrocyte P5N from 21-day-old rat pups were determined and were related to blood lead concentrations ascertained by atomic absorption spectrophotometry. Acute lead administration to rat pups resulted in a 16% to 21% reduction in erythrocyte P5N, with mean blood lead levels ranging from 77 to 108 μg/dl 24 hours later. Inhibition of erythrocyte P5N was linearly related to blood lead level (r = ?0.67, P < 0.05) following acute lead administration. Lead acetate addition to RBC preparations from 21-day-old rats resulted in concentration-dependent P5N inhibition which was comparable to that produced following acute in vivo exposure. The results indicate that acute P5N inhibition in lead-treated neonatal rats is due to noncompetitive P5N inhibition by lead. The inhibition of P5N produced by acute lead treatment is linearly related to blood lead concentrations.