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PubMed1980

Aldrin epoxidation catalyzed by purified rat-liver cytochromes P-450 and P-448. High selectivity for cytochrome P-450.

Aldrin epoxidation was studied in monooxygenase systems reconstituted from purified rat liver microsomal cytochrome P-450 or P-448, NADPH-cytochrome c reductase, dilauroylphosphatidylcholine and sodium cholate. Cytochrome P-450, purified from hepatic microsomes of phenobarbital-treated rats, exhibited a high rate of dieldrin formation. The low enzyme activity observed in the absence of the lipid and sodium cholate was increased threefold by addition of dilauroylphosphatidylcholine and was further stimulated twofold by addition of sodium cholate. The apparent Km for aldrin in the complete system was 7 +/- 2 microM. SKF 525-A, at a concentration of 250 microM, inhibited aldrin epoxidation by 65%, whereas 7,8-benzoflavone had no inhibitory effect at concentrations up to 250 microM. Addition of ethanol markedly increased epoxidase activity. The increase was threefold in the presence of 5% ethanol. When cytochrome P-448 purified from hepatic microsomes of 3-methylcholanthrene-treated rats was used, a very low rate of epoxidation was observed which was less than 3% of the activity mediated by cytochrome P-450 under similar assay conditions. Enzyme activity was independent of the lipid factor dilauroylphosphatidylcholine. The apparent Km for aldrin was 27 +/- 7 microM. The modifiers of monooxygenase reactions, 7,8-benzoflavone, SKF 525-A and ethanol, inhibited the activity mediated by cytochrome P-448. The I50 was 0.05, 0.2 and 800 mM, respectively. These results indicate that aldrin is a highly selective substrate for cytochrome P-450 species present in microsomes of phenobarbital-treated animals and is a poor substrate for cytochrome P-448. The two forms of aldrin epoxidase can be characterised by their turnover number, their apparent Km and their sensitivity to modifiers, like 7,8-benzoflavone and ethanol.

Aldrin↗
PubMed1990

[Acute poisoning by aldrin: relationship between serum levels and toxic effects in humans].

In the attempt to correlate clinical findings with serum levels of aldrin, sixteen patients were followed-up after acute intoxication by this agent. Eight of them, males and females, aged from 1 to 37 years, presented no or light symptoms (some discomfort and nausea). The serum of one of these patients was found to contain 16.6 ppb of aldrin and that of another, 1.41 ppb of dieldrin. A group of five patients, aged from two to 30 years, showed symptoms of moderate severity, reporting nausea, vomiting, drowsiness, dyspnea, sweating, mild jerking, rise in blood pressure and convulsions. Of these cases, two were accidental and three were attempted suicides, the majority achieving complete recovery within 24 hours. Serum levels of aldrin were between 6.98 ppb and 26.3 ppb and of dieldrin between 82.00 and 314.18 ppb. We found three severe cases, aged from 21 to 35 years, two attempted suicides and one occupational case. Two of these patients died and one of them presented hypothermia, coma, absence of reflexes and generalized convulsions, and another presented abdominal pain, paleness, sweating, cold extremities, dyspnea, hyperthermia and generalized convulsions. In the first one that died the serum levels were: of aldrin 30.00 ppb and of dieldrin 720 ppb. In the other levels of 747.3 ppb of aldrin and 1,314.00 ppb of dieldrin were found. The third had less serious symptoms and presented serum levels of aldrin of 31.05 ppb and of dieldrin 147.11 ppb.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMedDate not supplied

Aldrin epoxidation. Catalytic potential of lipoxygenase coupled with linoleic acid oxidation.

Epoxidation of aldrin was studied using highly purified soybean lipoxygenase in the presence of linoleic acid. Dieldrin, the primary stable reaction product, was quantified by electron-capture gas chromatography. The oxidation of aldrin to dieldrin was dependent on the concentration of linoleic acid, aldrin, and enzyme. The epoxidation was linear with time and exhibited a pH optimum of 7.4. The optimal conditions to observe maximum enzyme velocity included the presence of 0.25 mM linoleic acid, 200 microM aldrin, and 20 nM enzyme. Lipoxygenase inhibitors nordihydroguaiaretic acid, phenidone, 5,8,11-eicosatriynoic acid, and 5,8,11,14-eicosatetraynoic acid significantly inhibited epoxidation in a dose-dependent manner. Catalytic potential of lipoxygenase as expressed in terms of its turnover numbers was approximately 4.0 nmol/min/nmol of enzyme, and it appears that lipoxygenase is up to 20 times a better catalyst of aldrin epoxidation than cytochrome P-450. These results suggest that lipoxygenase, which is widely distributed in plants and animals, may represent yet another important pathway for epoxidation of aldrin.

Aldrin↗
PubMed1977

Fate of [14C]aldrin in crop rotation under outdoor conditions.

[14C]Aldrin was applied to soils (about 3kg/ha) in outdoor boxes at various locations (Germany, England, and United States), and crops were cultivated (maize, wheat, sugar beets, and potatoes). In the following year, crop rotation experiments were carried out in the same soils without retreatment; in addition, wheat was grown in soils retreated with [14C]aldrin (3.5 kg/ha). After the harvest of both years, the distribution of aldrin and major metabolites (dieldrin; photodieldrin; hydrophilic metabolites including dihydrochlordene dicarboxylic acid; an unidentified nonpolar compound X; and unextractable metabolites) was determined in plants, soils, and leaching water. Two further conversion products, photoaldrin and aldrin-trans-diol, occurred in trace amounts only in a few samples. Metabolic pathways for aldrin under outdoor conditions are presented. The distribution of radioactive residues in soils and plants as well as their quantitative chemical composition are discussed, and comparisons are made between the different experimental sites, the crops, the first and second year, and retreated and nonretreated samples. The quantitative results are compared to those of field trials.

Agriculture↗
PubMed1989

Effects of long-term aldrin administration on seizure susceptibility of rats.

The effects of long-term administration of sub-convulsive doses of aldrin, an organochlorinated pesticide, on seizure susceptibility of rats were studied. Results show that treatment with the pesticide made the rats more susceptible to sound-induced seizures; an increment in post-seizure depression time after maximal electroshock administration was also observed in aldrin-treated animals. Aldrin administration displaced the control dose-response curves constructed for amphetamine and pentylenetetrazol to the left and right, respectively; no differences were detected between control and aldrin-treated rats for strychnine, picrotoxin or 3-mercaptopropionic acid. The results, discussed in the light of the effects of aldrin on biogenic amines or on the electrophysiology of neurones suggested an involvement of both noradrenergic and alteration excitability of the CNS with the observed increments on seizure susceptibility.

Acoustic Stimulation↗
PubMed1992

Aldrin and dieldrin residues in human fat, milk and blood serum collected from Delhi.

1. Aldrin and dieldrin residues were monitored in the fat, breast milk and blood serum from female residents of Delhi. 2. The average aldrin and dieldrin contents were 0.048 and 0.099 ppb in adipose tissue, 0.003 and 0.060 ppb in breast milk and 0.004 and 0.002 ppb in blood serum, respectively. 3. The older donors contained higher levels of aldrin and dieldrin in their adipose tissue. 4. Primagravidae contained more of these chemicals in their breast milk. 5. A positive correlation was observed between the aldrin concentration in adipose tissue and breast milk, and that in adipose tissue and blood serum. Similarly, a significant correlation was found between dieldrin in adipose tissue and blood serum. 6. The levels of aldrin and dieldrin were low in samples from residents of Delhi when compared to those in developed countries.

Adipose Tissue↗
PubMed1980

Aldrin epoxidase activity in developing rabbit lung.

Pulmonary aldrin epoxidase activity was determined in 2-, 4-, 6-, 8-, 12-, and 16-week-old male rabbits using isolated perfused lung preparations and in vitro incubation techniques. In the perfusion experiments, it was determined that aldrin epoxidase activity increased with age up to 12 weeks of age. Although there was an increase in the weight of lungs with age, this did not appear to be related to the increase in aldrin epoxidation. In vitro experiments carried out using the same substrate to tissue ratio failed to exhibit an age-related increase in the aldrin epoxidase activity. Extrapolated values for aldrin epoxidation from in vitro experiments yielded much higher values than realized from perfusion experiments. Accessibility of the substrate to the enzymatic sites, saturation of the accessible enzyme system, and limiting availability of the cofactor necessary for the oxidative reaction remain as the possible mechanisms for the discrepancy between perfusion and in vitro incubation studies.

Age Factors↗
PubMed1988

Effect of aldrin on spermatogenesis, plasma gonadotrophins and testosterone, and testicular testosterone in the rat.

Quantitative evaluation of the different varieties of germ cells at stage VII of the seminiferous epithelium cycle, namely type-A spermatogonia (ASg), preleptotene spermatocytes (pLSc), mid-pachytene spermatocytes (mPSc) and step 7 spermatids (7Sd), along with radioimmunoassay of plasma gonadotrophins (FSH and LH), testosterone and testicular testosterone were performed in Wistar rats following treatment with aldrin (polycyclic chlorinated hydrocarbon insecticide) for approximately one (13 days) or two cycles (26 days) of the seminiferous epithelium. Extensive degeneration of all varieties of germ cells at stage VII, reduction in the sperm count and significant reductions in plasma concentrations of LH and testosterone were observed following aldrin treatment. The reduction in plasma concentrations of FSH was statistically significant only after treatment for two cycles. The inhibitory effect of aldrin on plasma gonadotrophins, testosterone levels, testicular testosterone content and numbers of 7Sd and ASg was maximum after treatment for two cycles. Administration of human chorionic gonadotrophin along with aldrin treatment for two cycles partially prevented the degeneration of germ cells and enhanced testosterone production. The results indicate that aldrin may have a direct inhibitory influence on gonadotrophin release, but the possibility of a direct action of the insecticide at the level of the testes is also discussed.

Aldrin↗
PubMedDate not supplied

Uptake and disposition of aldrin and dieldrin by isolated perfused rabbit lung.

The uptake, metabolism, and release of aldrin and dieldrin by the lungs were studied by use of isolated perfused rabbit lungs that were artificially ventilated and perfused through the pulmonary artery. Both recirculating and single-pass experiments were conducted using an artificial medium as perfusate. Aldrin accumulated in the lung from the perfusate through two distinct phases of uptake: a rapid phase involving simple diffusion and nonspecific binding and a slower phase representing its metabolic turnover as dieldrin. Dieldrin was not metabolized but accumulated in the lungs by a saturable and a nonsaturable process. Single-pass experiments with aldrin indicated that the initial velocity of uptake could be fitted to one component and a constant representing the rate of metabolism. Uptake of dieldrin was biphasic: one phase independent of the perfusate concentration and the other saturable with respect to the perfusate concentration. By the application of Michaelis-Menten kinetics, the maximum amount of dieldrin accumulation attributable to the saturable component was calculated to be 0.64 mumol/lung. Our results indicate that the accumulation of these chlorinated xenobiotics takes place through the processes of simple diffusion followed by nonspecific tissue binding. There was no evidence for irreversible binding of aldrin or dieldrin, its epoxide, in the lung. While the lung plays a role in metabolizing aldrin to dieldrin followed by a transient storage, neither substrate has the potential for long-term storage in the lung.

Aldrin↗
PubMed1992

Relative toxicity of aldrin, fenvalerate, captan and diazinon to the freshwater food-fish, Clarias batrachus.

The median lethal concentrations (LC50S) of aldrin, fenvalerate, captan and diazinon were determined for Clarias batrachus by trimmed Spearman-Karber method. The potency ratios of toxicity among them were analysed by parallel-line bioassay with quantal responses. The LC50S for 40 day of exposure of aldrin, fenvalerate, captan and diazinon were 0.00036, 0.0094, 0.5473 and 2.4186 ppm respectively. These values were lower than those obtained for an exposure of 96 hour. It shows the greater toxicity of the pesticides in a long-term exposure. The relative toxic potency of aldrin fenvalerate, captan and diazinon was in a ratio of 6807:241:4:1 respectively. Thus the chemically different groups of pesticides exhibit an order of toxicity as aldrin greater than fenvalerate greater than captan greater than diazinon for the freshwater catfish, Clarias batrachus. It infers that the catfish is most sensitive to aldrin and least sensitive to diazinon. The comparison of the sensitivity of various species tested against these pesticidal chemicals has also been done to review the available information.

Aldrin↗
PubMed1983

Differences in the biochemical properties of aldrin epoxidase, a cytochrome P-450-dependent monooxygenase, in various tissues.

Aldrin epoxidase, a cytochrome P-450-dependent monooxygenase, was studied in the lung and kidney of male rats. The sensitivity of the liver enzyme activity to different chemicals in vitro was influenced by the treatment of the animals with phenobarbital or methylcholanthrene. These results confirm that more than one form of cytochrome P-450 supports aldrin epoxidase in the liver. The lung and kidney aldrin epoxidase activity was not modified by the administration of chemical inducers to the rats. In vitro, the lung and kidney aldrin epoxidase activities were activated by tetrahydrofurane and progesterone, respectively. The results obtained from the lung and kidney indicate that one single species of cytochrome P-450, associated with aldrin epoxidase, exists in these organs, but it may be a different type, or regulated in a different manner in these tissues.

Adrenalectomy↗
PubMed1983

Identification of the cyanopregnenolone-inducible form of hepatic cytochrome P-450 as a catalyst of aldrin epoxidation.

In light of recent suggestions that hepatic microsomal aldrin expoxidation activity selectively reflects the phenobarbital (PB)-inducible form(s) of cytochrome P-450 (P-450PB), we tested the effect of pregnenolone-16 alpha-carbonitrile (PCN), a synthetic steroid that induces P-450PCN, a form of the cytochrome biochemically and immunochemically distinguishable from P-450PB. In hepatic microsomes prepared from rats receiving PB, 3-methylcholanthrene (3-MC), or PCN, the latter compound produced a greater increase in aldrin epoxidation activity relative to control than did PB, whereas 3-MC decreased enzyme activity. Moreover, the aldrin epoxidation activity in microsomes prepared from PCN- or PB-pretreated rats was selectively inhibited by form-specific antibodies directed against P-450PCN or P-450PB, respectively, whereas anti-P-450MC antibodies gave no inhibition with microsomes prepared from induced or control animals. We conclude that P-450PCN, P-450PB, and probably other cytochromes P-450 catalyze aldrin epoxidation, precluding use of this enzyme as a specific marker of a single form of the cytochrome.

Aldrin↗
PubMed1975

Excitatory and depressant effects of dieldrin and aldrin-transdiol in the spinal cord of the toad (Xenopus laevis).

An investigation was made into the action of the insecticide dieldrin and one of its metabolites, aldrin-transdio, on the isolated spinal cord of the toad, Xenopus laevis. Conventional electrophysiological techniques were used for stimulating and recording of dorsal and ventral spinal roots. An augmentation of polysynaptic reflex activity along with a marked reduction of orthodromic postsynaptic inhibition could be demonstrated in preparations isolated from dieldrin-poisoned animals. However, application of dieldrin to the isolated spinal cord failed to produce any significant effect. Application of aldrin-transdiol, on the other hand, caused a potentiation of spinal reflex activity and an increase in spontaneous activity of ventral and dorsal roots. Aldrin-transdiol also produced a marked reduction of spinal inhibitory mechanisms. The excitatory effects of aldrin-transdiol were followed by a strong depressant action on spinal excitability.

Aldrin↗
PubMed1992

Effects of endosulfan and aldrin on muscle coordination and conditioned avoidance response in rats.

The deteriorative effects after chronic endosulfan exposure on muscle coordination, learning and memory of rats were compared with that produced by aldrin which has been reported to have similar effects in experimental animals. A rota-rod apparatus was used to study the muscle coordination and learning and memory were tested by recording the response to unconditioned and conditioned stimuli using a pole-climbing apparatus. Aldrin but not endosulfan inhibited motor coordination in both sexes. A greater motor deterioration occurred in male group. This finding, together with the previous data which shows inhibition by its metabolite of motor activity, suggests that its metabolic product is responsible for this action. Like aldrin, endosulfan inhibited both learning ability and conditioned avoidance response. A change in the activities of brain monoamines or inhibition of perception and reflexes or both were proposed for these behavioural effects, since the former was reported to be produced by both compounds and the latter was found to occur in aldrin treated rats.

Aldrin↗
PubMedDate not supplied

Effect of aldrin on accessory sex glands and plasma testosterone levels in rats.

The effects of aldrin, an organochlorine insecticide, on accessory sex glands and plasma testosterone levels in rats were studied. The aldrin was administered i.p. for 13 days and 26 days at a dose of 150 micrograms/kg. Relative weights of prostate, seminal vesicles and coagulating glands were significantly decreased in the treated rats compared to those in controls. In addition, there was a significant fall in acid phosphatase activity in prostate and fructose content in accessory sex glands was also observed in treated animals. Plasma testosterone values showed a decrease with the duration of treatment. HCG supplementation with aldrin treatment prevented all those untoward effects of aldrin in experimental rats.

Acid Phosphatase↗
PubMed1981

Effect of parathion and aldrin on survival, ovarian 32P-uptake and gonadotrophic potency in a freshwater catfish, heteropneustes fossilis (Bloch).

The effects of insecticides containing either an organophosphate parathion (Paramar M 50) or an organochlorine aldrin (Aldrin) on the survival, ovarian 32P-uptake and the gonadotrophic potency of the pituitary gland and blood serum in Heteropneustes fossilis were studied for 4 weeks. Aldrin was found to be more Paramar M 50. Reduced ovarian 32P uptake and a significantly decreased level of total gonadotrophin in the pituitary gland and blood serum were seen when fish were kept either in SC (safe concentration) or in LC(I)50 (a concentration that had been found to kill half the fish in 96 h) of Aldrin and Paramar M 50. The data suggest that those insecticides retarded gonadotrophin secretion which in turn reduced ovarian 32P uptake.

Aldrin↗
PubMed1998

Does magnesium chloride modify aldrin-induced neurotoxicity in rats?

Magnesium chloride (MgCl2) has been proposed for the treatment of seizures of different etiologies. The present study investigated the effect of MgCl2 on aldrin-induced seizures. Initially, 50 male rats received 60 mg aldrin/kg po and the effects were classified as muscular twitches, clonic convulsions or tonic-clonic convulsions. Another group of 40 rats dosed with 60 mg aldrin/kg po received 0, 4, 8, or 12 mg MgCl2/kg i.m. The percentage of tonic-clonic convulsant rats that resulted from MgCl2 treatment were 90% at 0 mg/kg, 50% at 4 mg/kg, 40% at 8 mg/kg and 20% at 12 mg MgCl2/kg. The percentage of survivors in the group receiving 12 mg MgCl2/kg was 80% while the control group had 20% survival. The clonic convulsions were not modified by MgCl2 treatment. Blood and brain concentrations of aldrin and dieldrin (metabolite of aldrin) did not differ among groups. The MgCl2 administration decreased the neuroexcitability induced by aldrin and increased survivability.

Aldrin↗
PubMed1987

Aldrin epoxidase activity in liver microsomes from normal or streptozotocin-diabetic rats: comparison with activity in isolated hepatocytes from normal rats incubated with glucagon.

Aldrin epoxidase activity in liver microsomes from streptozotocin-diabetic rats is only 40% of that from normal rats. Epoxidation of aldrin has also been assayed in freshly isolated hepatocytes from normal rats. Addition of 10(-7) M glucagon to the incubation medium leads to a decreased aldrin epoxidase activity. Owing to the previously reported phosphorylation of a purified cytochrome P-450 isozyme, it is postulated that the cytochrome P-450 dependent aldrin epoxidase may be regulated by a glucagon induced phosphorylation process.

Animals↗