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Biomedical subjects

M Lotti

Publications and source records attributed to M Lotti.

At least 91 records · Page 5Linked to original sources
PubMed1983

Meperidine carboxylesterase in mouse and human livers.

Meperidine carboxylesterase activity was assayed in subcellular fractions of mouse and human liver by coupling the hydrolytic production of ethanol to the reduction of a tetrazolium dye. In mouse liver, the activity was found to be distributed among the mitochondrial, light mitochondrial, and microsomal fractions, whereas in human liver activity was found only in the microsomal fraction. The meperidine carboxylesterases in mouse liver and human liver were inhibited by two irreversible serine hydrolase inactivators (diisopropyl fluorophosphate and paraoxon) and by a reversible transition state analog (trifluoromercaptophenylacetone). Compared to the activities in mouse and human liver microsomes, the activity in mouse liver mitochondria was highly sensitive to the three inhibitors.

Acetone↗
PubMed1983

Characterisation of a mutant from Escherichia coli lacking protein L15 and localisation of protein L15 by immuno-electron microscopy.

Two mutants lacking protein L15 from the ribosome as determined by two dimensional gels were investigated using a number of different immunological methods. One strain was found to possess several protein L15 moieties which differed in net charge and in size. The other showed no evidence of L15 cross-reacting material (CRM) on the ribosome or in the supernatant. Ribosomes of this strain were used as a control in the process of the localisation of protein L15 on the surface of the large subunit of Escherichia coli ribosomes. Antigenic determinants mapped in the angle between the central protuberance and the L1 protuberance. Protein L15 has been assigned a central role in the large subunit in vitro assembly map, in peptidyltransferase activity and in the binding of erythromycin, so the significance of a mutant lacking this protein is discussed.

Bacterial Proteins↗
PubMed1982

Treatment of acute organophosphate poisoning: evidence of a direct effect on central nervous system by 2-PAM (pyridine-2-aldoxime methyl chloride).

Management of acute organophosphate poisoning in man includes rapid treatment with atropine and oximes. Oximes are thought to be unable to enter the central nervous system. We describe a case of parathion poisoning in a 3-1/2 year-old child and the effect of treatment with oxime 2-PAM (34 mg/kg) on EEG activity and clinical symptoms. The prompt improvement of cortical electrical activity documented by EEG could not be explained by any improvement of circulatory or respiratory function and has to be considered a direct effect of oximes on the central nervous system.

Brain↗
PubMed1982

Occupational peripheral neuropathies.

Neither clinical nor laboratory evaluation can distinguish occupational neuropathies from neuropathies due to other causes. A worker may suffer either from mechanical injury of individual nerves or from a toxic polyneuropathy that is usually axonal in type. A thorough occupational and environmental history and the recognition of clusters of cases are important in determining the diagnosis. Electrophysiologic studies are helpful in detecting neuropathies in patients who have been occupationally exposed to neurotoxins but have no symptoms. Prevention of occupational neuropathies depends on clinical vigilance, industrial hygiene surveys, biologic monitoring and periodic examination of workers exposed to neurotoxic chemicals. The development of more sophisticated methods of prevention and early detection of peripheral nerve involvement depend on understanding the mechanisms of action of toxins and the pathophysiology of the lesions they cause.

Animals↗
PubMed1981

Enzyme studies with human and hen autopsy tissue suggest omethoate does not cause delayed neuropathy in man.

Levels of acetylcholinesterase and neurotoxic esterase were measured in brain autopsy material. In tissue from a fatal human poisoning and from hens given 4-8 x unprotected LD50 AChE was highly inhibited and neurotoxic esterase uninhibited. The findings correlate with the inhibitory power of omethoate against these enzymes in vitro. It is concluded that omethoate has negligible potential to cause delayed neuropathy and a published report of human neuropathy due to omethoate is criticised.

Acetylcholinesterase↗
PubMed1981

Delayed neurotoxicity caused by a single massive dose of dichlorvos to adult hens.

A moderate neuropathic response was obtained in hens 2 weeks after being given a single massive s.c. dose of dichlorvos (100 mg/kg of active ingredient in a commercial 50% formulation). 1 day after dosing inhibition of neurotoxic esterase in peripheral nerve was 79-90%, in spinal cord 70-81% and in brain 89-92%. It is unlikely that repeated exposure of man to dichlorvos could cause neuropathy except at doses causing severe cholinergic effects at every exposure.

Animals↗
PubMed1980

Repeated small doses of a neurotoxic organophosphate. Monitoring of neurotoxic esterase in brain and spinal cord.

The effects of small repeated oral doses of mono-2-cresyl diphenyl phosphate (MOCP, 2.5 mg/kg/day) on hen brain and spinal cord neurotoxic esterase (NTE) were measured. The enzyme levels were depressed to about 40% and 55% of normal respectively and maintained at that level for 8 weeks. No clinical and only doubtful histological signs of neuropathy were detected. Neuropathy could be precipitated by depressing the level to < 20% either with a single high dose (50 mg/kg), or by an increase of the repeated dose level to 5 mg/kg/day. There was no correlation between inhibition of NTE in the nervous tissue and the "NTE-like" activity in lymphocytes. "NTE-like" activity in spleen was consistently inhibited but to a lesser extent than that in the brain or spinal cord. Brain AChE and BuChE were not affected.

Acetylcholinesterase↗
PubMed1980

Delayed neurotoxicity caused by chronic feeding of organophosphates requires a high-point of inhibition of neurotoxic esterase.

Experiments are reported showing that chronic feeding of either mono-2-cresyl diphenyl phosphate or diisopropyl phosphorofluoridate (DFP) to hens does not cause clinically observable delayed neurotic effects prior to a point when inhibition of neurotoxic esterase (NTE) of brain and spinal cord reaches 70-90%. These results are contrary to another study with diisopropyl phosphorofluoridate, which claims neuropathy without high inhibition, but are supported by results of chronic feeding experiments with tri-o-cresyl phosphate. The discrepancy cannot be attributed to differences in the strains of hens used.

Animals↗
PubMedDate not supplied

Distribution and some biochemical properties of rat paraoxonase activity.

The calcium-dependent enzyme activity which hydrolyzes the p-nitrophenyl-O-P bond of paraoxon (paraoxonase) has been studied in several rat and human tissues. Rat plasma and liver showed the highest activities (1.31 +/- 0.19, 0.82 +/- 0.09 nmol/min mg protein +/- SEM, respectively), while other tissues showed less than 2% plasma activity. The Arrhenius plot showed monophasic patterns in both tissues with activation energy values of Ea = 57 +/- 3 and 69 +/- 4 kcal/mol degree K for rat liver and plasma, respectively. Rat plasma and liver paraoxonase lost about 80% activity after 24-hr storage at 27-30 degrees C and was not restored by calcium addition. There was no loss of activity in human serum after 3 days and only 33% after 5 days. The pH optimum for paraoxonase activities was about 7.4 for both rat tissues. It is concluded that plasma paraoxonase is similar to the liver enzyme and is a good mirror for total body detoxifying activity.

Animals↗