curcumin and Poisoning

This review deals with the three candidate compounds which may combat with dioxins' toxicity. Geranylgeranylacetone (GGA), an antiulcer drug, counteracts suppression of body weight gain and lethality produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in C57BL/6J mice. Similarly, curcumin, a food ingredient anticipates the TCDD's toxicity on body weight gain. Both GGA and curcumin had no effect on the induction of hepatic ethoxyresorufin O-deethylase activity by TCDD. These data suggest that both compounds exhibit a protective effect against some forms of dioxin toxicity by a mechanism without involving inhibition of aryl hydrocarbon receptor activation. Further, the mechanism involved in resveratrol action on dioxin's toxicity was also discussed. Prior to the application of these compounds to Yusho patients, the limitation and possibility of these candidate compounds are seemed to be further studied.

Topics: Animals; Anti-Ulcer Agents; Curcumin; Cytochrome P-450 CYP1A1; Diterpenes; Food Contamination; Humans; Mice; Mice, Inbred C57BL; Oryza; Plant Oils; Poisoning; Polychlorinated Biphenyls; Polychlorinated Dibenzodioxins; Receptors, Aryl Hydrocarbon; Resveratrol; Stilbenes

The aim of this study was to compare the protective effects of curcumin, curcumin-β-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.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; beta-Cyclodextrins; Central Nervous System Diseases; Curcumin; Dimethylhydrazines; Dose-Response Relationship, Drug; gamma-Aminobutyric Acid; Hippocampus; L-Lactate Dehydrogenase; Liver; Male; Mice; Mice, Inbred ICR; Nanoparticles; Particle Size; Poisoning

Formaldehyde is a common environmental contaminant that causes oxidative DNA damage in cells by increasing the production of reactive oxygen species. The aim of this study was to investigate the amount of 8-hydroxy-deoxyguanosine (8-OhdG), tumor protein 53(TP53), beta-amyloid[Aß(1-42), Aß (1-40)], total antioxidant capacity (TAC) and malondialdehyde (MDA) and the therapeutic role of curcumin in rat cells with oxidative DNA damage caused by formaldehyde.. The control group was given physiological saline for 15 days (i.p.) and the second group was given 37% formaldehyde (i.p.) at a dose of 9 mg/kg group every other day. The third group was given 9 mg/kg formaldehyde (i.p.) every other day and treated therapeutically with 100 mg/kg curcumin every day by gavage. At the end of the trial period, urine, blood, and brain tissue was collected from the rats.. The levels of MDA in sera were increased and the TAC, TP53, and Aß (1-40) levels were reduced in the formaldehyde-treated group with respect to the control group (p<0.005). After treatment with curcumin, the levels of sera MDA were significantly reduced, the TAC, TP53, and Aß (1-40) levels were significantly increased (P < 0.05). The levels of whole brain Aß (1-42) and 8-OhdG were increased in the formaldehyde-treated group and reduced after treatment with curcumin (P < 0.05). Urinary 8-OhdG excretion increased in the formaldehyde-treated group (P < 0.05) and decreased after treatment with curcumin (P > 0.05).. In conclusion, the oxidative stress caused by formaldehyde exposure was reduced with the application of curcumin.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Administration, Oral; Amyloid beta-Peptides; Animals; Antioxidants; Blood Chemical Analysis; Brain; Curcumin; Deoxyguanine Nucleotides; Disease Models, Animal; DNA Damage; Formaldehyde; Poisoning; Rats; Treatment Outcome; Urine

To evaluate the potential of curcumin on toxic and carcinogenic effects of Aflatoxin B1 (AFB1) in relation to AFB1 metabolism, we studied the effects of curcumin on hepatic AFB1-DNA adduct formation and glutathione S-transferase (GST) activity, and the toxic effects of AFB1 in male Fischer 344 rats. Oral administration of curcumin to 5-week-old male rats at a dose of 8 or 80 mg/kg for five consecutive days for three weeks resulted in reduction of AFB1-DNA adduct formation mediated by both liver microsomal and postmitochondrial fractions. The activity of liver GST toward a universal substrate, CDNB, was increased in curcumin-administered rats. As for the acute toxicity of AFB1, curcumin was orally administered to rats for 3 weeks and then AFB1 was given by intragastric intubation. The result showed a decrease of plasma AST and ALT activities in curcumin-treated rats compared with those which received AFB1 alone. Moreover, we have observed that curcumin also reduced glutathione S-transferase placental form positive single cells and foci caused by AFB1 treatment. These results demonstrate the potential of curcumin to reduce the toxic and carcinogenic effects of AFB1 by modulating hepatic drug metabolizing enzymes responsible for AFB1 metabolism.

Topics: Administration, Oral; Aflatoxin B1; Animals; Carcinogens; Curcumin; Disease Models, Animal; DNA Adducts; Enzyme Inhibitors; Glutathione Transferase; Liver; Male; Mutagens; Poisoning; Rats, Inbred F344