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4 hydroxyanisole/emorragia

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Lung hemorrhagic toxicity of butylated hydroxyanisole in the rat.

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Male Sprague-Dawley rats were injected intraperitoneally (i.p.) with butylated hydroxyanisole (BHA) at doses of 0, 1, 4, 16, 64, 256, 384, 576, 864, 1296 and 1944 mg/kg/day for 7 days. Deaths occurred in a dose- and time-dependent manner when BHA was given in amounts greater than 576 mg/kg. The LD50
A carcinogenicity study on butylated hydroxyanisole (BHA) was carried out in Japanese house musk shrews (Suncus murinus) (suncus), which have no forestomach. BHA was mixed with the basal diet and was processed into pellets. One hundred and twenty-two female and 130 male suncus were maintained with a
3-tert-Butyl-4-hydroxyanisole and tert-butyl-hydroquinone (TBHQ) are antioxidants known to promote renal and bladder carcinogenesis in the rat, although the mechanisms of these effects are unclear. Because glutathione (GSH) conjugates of a variety of hydroquinones are nephrotoxic, and because

Antioxidants can prevent cerebral malaria in Plasmodium berghei-infected mice.

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A/J and CBA/H mice infected with Plasmodium berghei ANKA, a murine model of cerebral malaria, were used to see whether antioxidants influenced the outcome of this disease. Untreated, infected mice died 7 to 9 days after infection, often with cerebral symptoms. Haemorrhages, mononuclear infiltration
The comparative effects of the antioxidants, butylated hydroxyanisole (BHA), ethoxyquin, and cysteine on pyrrolizidine-alkaloid-induced (PA-induced) lethality and acute hepatotoxicity were assessed in female mice. Diets containing 0.75% BHA, 0.25% ethoxyquin, or 1% cysteine were fed to mice for 10 d

Studies on the role of lipid peroxidation in the acute toxicity of TCDD in rats.

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Lipid peroxidation has been shown to be enhanced following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but its role in TCDD toxicity is unclear. The present study was undertaken to further elucidate the relations between lipid peroxidation and TCDD lethality. A time course and

RIP1 and RIP3 mediate hemin-induced cell death in HT22 hippocampal neuronal cells.

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Intracerebral hemorrhage (ICH) is a devastating neurological injury associated with significant mortality. Necroptosis is a newly identified type of programmed necrosis initiated by the activation of tumor necrosis factor alpha. Evidences had demonstrated the importance of necroptosis
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