ABSTRACT
The aim of this study was to compare the protective effects of curcumin, curcumin-ß-cyclodextrin nanoparticle curcumin (BCD-CUR) and nanoliposomal curcumin (NLC) on unsymmetrical dimethylhydrazine (UDMH) induced poison in mice. Curcumin, BCD-CUR, and NLC were prepared and their properties of zeta potential, particle size, encapsulation efficiency, and loading capacity were characterized. Eighty-eight male ICR mice on normal chow diet were randomly divided into 11 groups, and intraperitoneally injected with UDMH alone, or together with different doses of curcumin, BCD-CUR or NLC daily for up to 10 d. Enzyme activities of serum alanine transaminase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) were analyzed by fully-automatic analyzer and neurotransmitter levels were determined with high performance liquid chromatography (HPLC). 150 mg/kg curcumin treatment alone significantly reduced levels of serum ALT and LDH that were induced by UDMH and markedly increased level of γ-amino butyric acid (GABA) that were reduced by UDMH in the hippocampus. 150 mg/kg BCD-CUR not only decreased significantly the increase of ALT, LDH and glutamate (Glu) but also recovered levels of AST and GABA. 150 mg/kg NLC recovered profoundly levels of AST and GABA while decreased remarkably the UDMH induced increase of ALT, LDH, Glu and 5-hydroxytryptamine (5-HT). In addition, treatments with all tested doses of NLC significantly reduced the UMDH induced dopamine (DA), the monoamine neurotransmitter. NLC had more profound protective effects against liver and central nervous system injury induced by UDMH than a suspension of BCD-CUR or curcumin did in mice.
Subject(s)
Curcumin/pharmacology , Dimethylhydrazines/poisoning , Nanoparticles/chemistry , Poisoning/drug therapy , beta-Cyclodextrins/chemistry , Alanine Transaminase/blood , Animals , Aspartate Aminotransferases/blood , Central Nervous System Diseases/chemically induced , Central Nervous System Diseases/drug therapy , Curcumin/chemistry , Dose-Response Relationship, Drug , Hippocampus/drug effects , Hippocampus/metabolism , L-Lactate Dehydrogenase/blood , Liver/drug effects , Liver/metabolism , Male , Mice , Mice, Inbred ICR , Particle Size , gamma-Aminobutyric Acid/bloodABSTRACT
Studies of serum proteins modifications both spontaneous and catalyzed by metals in rats under single exposure to nonsymmetric dimethylhydrazine revealed reliable, significant increase in oxidative destruction of proteins. That proves deep peroxidative syndrome in the experimental animals.
Subject(s)
Blood Proteins/drug effects , Dimethylhydrazines/poisoning , Occupational Diseases/blood , Oxidative Stress/drug effects , Animals , Blood Proteins/metabolism , Disease Models, Animal , Female , Male , Occupational Diseases/chemically induced , RatsABSTRACT
OBJECTIVE: To investigate the characteristics and mechanism of the acute and chronic injuries induced by unsymmetrical dimethylhydrazine (UDMH). METHODS: A total of 128 male rats were randomly divided into four groups: UDMH intoxication acute response group and chronic response group, and corresponding control groups. UDMH was administrated through inhalation at the concentration of 8x10(-4)g/m(3) for 15 minutes. Animals of each group were sacrificed at 3, 6, 12, 24, 48 and 72 hours respectively after the intoxication. Pathologic changes and blood gas were examined. Chronic injuries and pathologic changes were also observed 1 year after the intoxication. RESULTS: Major pathological changes in the intoxication group were cerebral edema, degeneration and necrosis of neuron, enlargement and hemorrhage of capillary. Damages of different degree were found in liver, kidney, lung, heart, spleen, stomach, intestine, thymus, blood, bone marrow. Pallium ischemia was also found in the intoxicated rats 1 year after the intoxication, including ischemia damage of neuron in cerebral cortex, hemorrhage and focal liquefaction of thalamus and medulla conducting bind, dissociation, rupture, not uniform circuitry in conducting fibers. CONCLUSION: Our study reveals the basic pathological induced by intoxication of UDMH. The most severe stage of the injury appears 2-6 hours after intoxication. Long term investigation reveals pallium ischemia, thalamus hemorrhage and liquefaction in the medulla oblongata 1 year after the intoxication with UDMH. All the changes are significant.
Subject(s)
Central Nervous System/pathology , Dimethylhydrazines/poisoning , Animals , Central Nervous System/drug effects , Disease Models, Animal , Male , Poisoning/pathology , Random Allocation , Rats , Rats, Wistar , Time FactorsABSTRACT
The authors analyze emotional features in workers with occupational exposure to hydrazines, hydrocarbons and nitroglycols. Chronic occupational poisoning with those chemicals induce numerous emotional symptoms that are specific and varying in severity. The materials presented by authors could be interesting for occupational therapist, internist and psychiatrist for early diagnosis of chronic occupational intoxications, treatment of emotional disorders in workers and better occupational safety.
Subject(s)
Dimethylhydrazines/poisoning , Ethylene Glycols/poisoning , Hydrocarbons/poisoning , Mood Disorders/chemically induced , Mood Disorders/psychology , Occupational Diseases/diagnosis , Chronic Disease , Humans , Mood Disorders/diagnosis , Psychological Tests , Severity of Illness IndexABSTRACT
Comments are presented on a case history of extensive burns associated with 1,1-dimethylhydrazine (UDMH) toxicity in a 31-year-old man. Neurological symptoms dominated early developments. Specific treatment with pyridoxine, while begun late, effected a quite rapid resolution and the subsequent progression of treatment was straightforward. In reviewing previous reported findings, the authors have clarified the distinctive characteristics of UDMH toxicity, the methods for its detection and modes of treatment. They draw conclusions, based on problems encountered, linked to the exceptional character of acute UDMH toxicity especially in its association with extensive burns.
