No abstract

The dependence of fluorescent porphyrin levels on the concentration of lead in blood, liver and kidney has been examined as functions of both the level and duration of dosing. Individually housed male Wistar COBS rats of 200 g were randomly selected for 3, 7, 21 and 35 day dosing periods in groups of: control, 50, 100 and 1000 ppm dosing in drinking water. The plot of all data points for porphyrin concentration against measured lead burden covers the same range of levels and closely resembles the scatter of data observed in humans. However, subsets of this plot defined by individual dose levels and durations yield well-defined linear relationships. At all dose levels at 7 days the correlation of porphyrin concentration to lead tissue burden is negative in all tissues, showing a direct inhibition of hemopoiesis with lead burden. Depending on the tissue the slope becomes less negative, or, as in blood, positive at 21 and 35 days at all doses. This compensation is most rapid in blood, then liver and is least evident in kidney. The time at which compensation is observed is the same for all doses in each tissue and seems therefore, to depend on the rate of protein turnover in different tissue types. These results suggest that a direct correlation of porphyrin concentration to lead burden is not valid without knowledge of the dosing history. As well, evidence of compensation in one tissue does not imply successful compensation in other affected tissues where regeneration rates are slower.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

A study on rats of the effects of lead on delta-aminolevulinate dehydratase (ALA-D) activity, and its pH-dependent maximal enzyme activity is reported. Over a 5-week period, the lead burden and ALA-D activity in kidney, liver and brain are documented. Lead concentrations in the organs, expressed as micrograms/g protein are in the sequence kidney greater than liver greater than brain and reach essentially a constant level after 3 days of exposure. This is consistent with the existence of an efficient mechanism removing lead from these organs. Lead affects the ALA-D in all three organs by reducing the activity and shifting the pH of maximum enzyme activity to more acidic values. In common with the lead levels, the ALA-D activity does not deteriorate beyond the levels reached after 3 days of exposure. The existence of a mechanism removing lead from the organs is further supported in a recovery study on blood and kidney, in which both lead level and ALA-D activity return essentially to normal values after 7 days of no exposure to lead.