Antioxidants acute toxicity

Kakkar et al. (1992) exposed six male Wistar rats to a single nominal concentration of 15,302 ppm for 10 min the animals were sacrificed 24 h later. Earlier studies (not presented) had shown this to be the highest concentration tolerated without any mortality or acute toxicity. Biochemical changes in the brains of these rats suggested impairment of antioxidant defenses. No other signs of toxicity were reported. The exposure was performed under static conditions, and the measurement method was not described. 

The acute toxicity and carcinogenicity of Ni3S2 and Ni3S2-derived soluble nickel (Ni2+) in mice depend, in part, on the antioxidant capacity of target organs, which varies among different strains... 

Summing RB, Walton MF. 1973. Modification of the acute toxicity of mutagenic and carcinogenic chemicals in the mouse by prefeeding with antioxidants. Food Cosmet Toxicol 11 547-553. 

Recent studies have shown that cyanide also inhibits the antioxidant defense enzymes (such as catalase, superoxide dismutase, and glutathione peroxidase) and stimulates neurotransmitter release. These effects of cyanide may also contribute to its acute toxicity. The prolonged energy deficit and the consequent loss of ionic homeostasis, which may result in activation of calcium signaling cascade and eventually cell injury, contribute to cyanide toxicity resulting from subacute exposure or in the postintoxication sequela. 

Acute toxicity 54 Adhesives 5 Antioxidants 11 Anti-static agents 11 Articles 11, 13... 

The lipid peroxide stimulation mechanism of paraquat acute toxicity has been questioned by Shu et al. (1979), who have shown that it is possible by pre-treatment with N,ivr-diphenyl-p-phenylene-diamine, an antioxidant, to prevent the paraquat stimulation of lipid peroxidation without protecting the animals against its lethal effects. 

Carvacrol also improves cognitive activity. Azizi et al. [100] examined the effect of carvacrol and thymol in two rat models of dementia deficits caused by amyloid p and by scopolamine. The method they used was the Morris water maze test and they also assessed the acute toxicity of both carvacrol and thymol. The result showed that both substances could reverse and alleviate the induced cognitive impairments, for example, the escape latency and reduction in target quadrant entries. Both substances also were shown to be relative safe, with LD50s of thymol (565.7 mg/kg) and carvacrol (471.2 mg/kg) that were significantly higher than the therapeutic concentration. The authors also suggest that the antioxidative, antiinflammatory, and anti-choUnesterase activity could be involved in these activities. 

Sesamex [51-14-9] (Sesoxane) (30) is a synergist oflow toxicity, acute oral LD q (rat) = 2000 2270 mg/kg, for pyrethrins and allethrin. 6,7-Dihydroxy 4-methylcoumarin has been offered as an antioxidant for phenoHcs and polymers, and as an anthelmintic. 2,4,5-Trihydroxybutyrophenone has been available as an antioxidant and light stabilizer for polyolefins, waxes, and foods. Isoflavones, eg (31), have been patented as components of antioxidant compositions for foods and cosmetics (qv) (97). 

Gharbi N, Pressac M, Hadchouel M, Szwarc H, Wilson SR, Moussa F (2005) [60]Fullerene is a powerful antioxidant in vivo with no acute or subacute toxicity. Nano Lett. 5 2578-2585. 

Results from this study showed that SOD activity was not affected by acute ADR treatment. A second finding was that acute ADR toxicity did not promote cardiac lipid peroxidation. However, it was observed that mitochondrial lipid peroxidation was highest in mice fed diets low in both antioxidants. Ultrastructural examination revealed mitochondrial abnormalities in cardiac tissue from ADR-treated animals (Figures 3 and 4). There were large vacuoles within the mitochondria and condensation of the inner and outer membranes of the mitochondria. The ultrastructural effects of ADR treatment were most severe in the low E, Mn-deficient mice. It is reasonable to suggest that a higher than normal level of lipid peroxidation may predispose the animal to tissue damage from ADR. Consistent with this concept, Meyers et al. (34) have reported that pretreatment with supplemental vitamin E can reduce the toxicity of ADR in mice. 

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