The effect of experimental lead poisoning on some enzymatic activities of the kidney

Secchi, G. C.; Alessio, L; Cirla, A

doi:10.1016/0009-8981(70)90300-1

Cited by 11 publications

(6 citation statements)

References 16 publications

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“…Lactate dehydrogenase playes an important role in the intermediary metabolism as a link between amino acid metabolism and the citric acid cycle where it converts lactate into pyruvate. The increase in the activity of this enzyme due to lead intoxication in the present study is in agreement with the biochemical findings of Secchi 37) but in contradiction with the findings of Iannaccone et al, 33) where the activity of lactate dehydrogenase was unmodified in the kidney homogenate of rats fed for 6 months with 0.1 per cent lead acetate diet and of Yagminas et al,38) where the activity of this enzyme was lowered in the kidney of lead acetate treated rats. The varieties in the activity of renal dehydrogenases due to lead intoxication obtained by different investigators could be due to the variations in the experimental conditions such as the level of exposure, duration, route of administration and animal species used in the experiment.…”

Section: Discussionsupporting

confidence: 78%

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Histochemical Demonstration of the Alterations in the Renal Dehydrogenases Activities Induced by Lead in Wistar Albino Rats (Rattus norvegicus).

Jarrar

Mahmoud

2002

JOURNAL OF HEALTH SCIENCE

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A total of 112 male albino rats (Rattus norvegicus) were divided into seven groups and exposed to lead acetate trihydrate (0, 0.125, 0.25, 0.5, 1.0, 2.0 and 4 per cent for 1 to 8 months) in drinking water to investigate possible histochemical changes of nine renal dehydrogenases due to lead intoxication. A marked increase in the activity of lactate-, glucose-6-phosphate-, α-glycerophosphate-, reduced nicotinamide adenine dinucleotide (NAD)-and reduced nicotinamide adenine dinucleotide phosphate (NADP) dehydrogenase was observed while significant reduction was recorded in the activity of succinate-, malate-, isocitrate-and glutamate dehydrogenase. Changes in the activity of renal dehydrogenases were seen mainly in the pars recta and to a lesser extent in the pars convoluta and the ascending thick segment of the loop of Henle while the other medullary portions of the renal tubule were less affected. These histochemical findings led us to conclude that such changes in the renal dehydrogenases activities were due to chronic lead exposure and could be an adaptation to the metabolic, structural and functional alterations in the organelles of the renal cells especially the mitochondria.

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Section: Discussionsupporting

confidence: 78%

“…33,37) NAD-dependent isocitrate dehydrogenase is structuraly bounded to the mitochondria and participates in the Krebs cycle. It has been reported that the activity of this enzyme was increased in the muscle fibers of lead intoxicated rats.…”

Section: Discussionmentioning

confidence: 99%

Histochemical Demonstration of the Alterations in the Renal Dehydrogenases Activities Induced by Lead in Wistar Albino Rats (Rattus norvegicus).

Jarrar

Mahmoud

2002

JOURNAL OF HEALTH SCIENCE

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“…Howard (15) found increased erythrocytic glutathione reductase activity in lead exposed human subjects, and postulated that the increase is a compensatory mechanism and due to the removal of reduced glutathione. Secchi et al (28) found an increase in guinea pig renal lactate dehydrogenase (isoenzymes 4 and 5) and glucose 6 phosphate dehydrogenase activity after oral lead treatment. This pattern was identical to the enzymatic changes noted after experimental renal ischemia.…”

Section: Discussionmentioning

confidence: 99%

Effect of Lead Exposure on the Activity of Some Hepatic Enzymes in the Rat

et al. 1979

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SummarySeven-day-old rats were fed 1% lead acetate tetrahydrate solution for 2,4, or 7 days. Adult rats were fed the same lead solution for 6-8 wk. In the newborn rats, hepatic UDP-bilirubin glucuronyl transferase (GT) and gamma glutamyl transpeptidase (GGTP) activities were markedly increased. GT activity was increased after 4 days as compared to the controls (6.3 f 0.3 vs. 4.3 f 0.3, P < 0.001), and was maximal after 7 days of treatment (7.5 f 0.4 vs. 4.6 f 0.4, P < 0.001). GGTP activity was already maximally increased after 2 days of lead treatment (1.4 rt: 0.2 vs. 0.4 f 0.1, P < 0.001). Hepatic GT and GGTP activities were similarly increased in adult rats (7.9 f 0.3 vs. 5.1 f 0.1, P < 0.001, and 0.7 f 0.1 vs. 0.4 f 0.1, P < 0.005, respectively). In vitro studies adding lead citrate to liver homogenates did not produce any direct effect on GT and GGTP activities. SpeculationThe increase in hepatic GT and GGTP activities in lead treated animals appears to be a response to lead induced cellular damage or may result from interference with regulatory mechanisms responsible for production of these enzymes and not related to hepatic enzyme induction. The hepatic metabolism of drugs ingested by children with an increased lead burden may, therefore, be significantly altered.While lead remains one of the more important industrial and environmental toxins, and a series of recent factors have reduced the incidence of lead exposure and toxicity (1 I), its affect on the liver has received relatively little attention when compared to its impact on hematopoietic and neuromuscular systems. Lead administration to animals causes changes in the liver (12, 14) visible by light and electron microscopy. Additionally, it increases the concentrations of enzymes in serum released from damaged hepatocytes, and produces alterations in hepatocyte function as manifested by decreased bilirubin clearance and enhanced bromosulfophthalein retention (8,31). Recently, inhibition of the microsoma1 hepatic cytochrome P-450 dependent mixed function oxidase system has been reported (3, 26) in lead intoxicated animals and humans, suggesting the possibility of an alteration in hepatic drug metabolism. In order to explore further the effects of lead on hepatic enzyme activity, microsomal, noncytochrome P-450 dependent systems were studied in rats previously shown to be poisoned by lead (17). MATERIALS A N D METHODSanimals and littermate controls at 2,4, and 7 days were 12, 10; 8, 6; and 20, 18, respectively. All animals were killed by decapitation 24 hr after the last dose. The livers were removed, weighed, and the activity of UDP-bilirubin GT (EC 2.4.1.17), GGTP (EC 2.3.2.2), and hepatic protein content were determined. CHRONIC ADULT EXPOSUREFifteen adult male Sprague Dawley rats weighing 200-250 g were given a 1% lead acetate tetrahydrate solution in their daily drinking water for 6-8 wk. The lead solution was offered ad libitum. At the end of the treatment period, the rats were killed by decapitation, the livers were removed, weighed, GT and GGTP ...

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“…On the other hand, marked decrease in the content of both 125I-PTH and none-PTHbound 1251 in the kidney of SAT-treated rat suggests a possibility of the decrease in renal blood flow and resultant hypoxia which might have some influence on the decrease in that enzyme activity. (Secchi et al, 1970). Although, prolonged hypocalcemia might cause a fall of renal PTH'ase activity according to Ohata et al (1971), who found such decrease 3 weeks after parathyroidectomy, the decrease of serum calcium following SAT injection was too mild and transient to cause such decrease.…”

Section: Discussionmentioning

confidence: 99%

“…Renal injury causes a decrease and/or an increase in the activity of kidney enzyme, sometimes followed by an increase in the enzyme activity in plasma and/or urine. (Bastide and Bastide, 1969 ;Jurkiewicz et al, 1969;Secchi et al, 1970). While an increase in enzyme activity after renal injury has been considered as a metabolic adaptation of the kidney to a condition of tissue hypoxia in the initial phase of acute renal failure (Nielsen et al, 1968;Secchi et al, 1969), a decrease in enzyme activity in such state might be due to the irreversible changes of the cells responsible for its synthesis through a direct injury or secondary to hypoxia.…”

Section: Discussionmentioning

confidence: 99%

Effect of Renal Injury on the Activity of Enzymes Preferentially Hydrolyzing Parathyroid Hormone

et al. 1971

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The activity of enzymes preferentially hydrolyzing parathyroid hormone at pH 8.5 was markedly decreased in the supernatant of rat kidney homogenate centrifuged at 600g 24hr after the intraperitoneal injection of 0.5g/kg Na-Sulfacetylthiazole (SAT). The content of plasma 125I-PTH 30 min after the intravenous injection in SAT-treated rats was greater than that in control animals. The content of 125I-PTH and non-PTHbound 125I was marked ly decreased in the SAT-treated rat kidney as compared with that of controls but there was no difference in the ratio of 125I-PTH to non-PTH-bound 125I in the kidney between SAT-treated rats and control ones. The delayed disappearance of plasma 125I-PTH in SAT-treated rats than in controls might be related to the impairment of inactivation of PTH by the kidney due to the decrease of renal PTH'ase activity induced by SAT treatment.

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The effect of experimental lead poisoning on some enzymatic activities of the kidney

Cited by 11 publications

References 16 publications

Histochemical Demonstration of the Alterations in the Renal Dehydrogenases Activities Induced by Lead in Wistar Albino Rats (Rattus norvegicus).

Histochemical Demonstration of the Alterations in the Renal Dehydrogenases Activities Induced by Lead in Wistar Albino Rats (Rattus norvegicus).

Effect of Lead Exposure on the Activity of Some Hepatic Enzymes in the Rat

Effect of Renal Injury on the Activity of Enzymes Preferentially Hydrolyzing Parathyroid Hormone

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