Acute toxicity oftrans-5-hydroxy-2-nonenal in fisher 344 rats

  title={Acute toxicity oftrans-5-hydroxy-2-nonenal in fisher 344 rats},
  author={Akiyoshi Nishikawa and Rama S. Sodum and Fung-Lung Chung},
The potential toxicity oftrans-4-hydroxy-2-nonenal (HNE), a product formedin vivo during lipid peroxidation, which is also present in foods, was investigated in Fisher 344 rats. Five groups of five male rats each were given by gavage 1000, 300, 100, 30 or 10 mg/kg body weight HNE dissolved in 0.5 mL corn oil. The sixth group, the control, received corn oil alone. Two rats died 6 and 8 hr after being treated with 1000 mg/kg HNE. These two rats showed extensive acute tubular necrosis of the… 
Hepatotoxicity and Nephrotoxicity Produced by 4-Hydroxy-2-Nonenal (4-HNE) Following 4-Week Oral Administration to Sprague-Dawley Rats
It is demonstrated that oral daily exposure to 4-HNE for 28 d produced hepatotoxicity and nephrotoxicity, and the no-observed-adverse-effect level (NOAEL) for 4- HNE was calculated to be <0.5 mg/kg/d.
4-Hydroxynonenal (HNE), a Toxic Aldehyde in French Fries from Fast Food Restaurants
The toxic lipid peroxidation product, α,β,4-hydroxy-2-trans-nonenal (HNE) concentration, was measured in French fries (FF) from six local fast food restaurants. FF were purchased between 2 and 3 pm
Estimation of daily exposure to 4-hydroxy-2-alkenals in Korean foods containing n-3 and n-6 polyunsaturated fatty acids
Considering the basal level of 4-hydroxy-2-alkenals in many tissues, the present value from the diet may not pose a significant risk for human health.
Changes in markers of lipid oxidation and thermal treatment in feed-grade fats and oils.
PV, a marker for the primary phase of lipid oxidation, increased most in fish oil (FO), followed by tallow (TL), soybean oil (SO), linseed oil (LO) and modified algae oil (MAO), while palm oil (PO) showed no appreciable increase in PV.


Induction of liver tumors in F344 rats by crotonaldehyde.
Crotonaldehyde appears to be a weaker tumorigen than N-nitrosopyrrolidine, which suggests that alpha, beta-unsaturated carbonyl compounds, which are ubiquitous in the human environment and can be formed endogenously, may be an important class of potential carcinogens.
Cytotoxicity and metabolism of 4-hydroxy-2-nonenal and 2-nonenal in H2O2-resistant cell lines. Do aldehydic by-products of lipid peroxidation contribute to oxidative stress?
The results show that cell lines adapted and/or selected in a highly peroxidative environment are also resistant to the cytotoxicity of aldehydes formed during lipid peroxidation, possibly through the glutathione transferase system.
Nephrotoxicity of thiabendazole in mice depleted of glutathione by treatment with DL-buthionine sulphoximine.
  • T. Mizutani, K. Ito, H. Nomura, K. Nakanishi
  • Biology, Medicine
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • 1990
Metabolism of the lipid peroxidation product 4-hydroxynonenal by isolated hepatocytes and by liver cytosolic fractions.
The effective conversion of the cytotoxic 4-hydroxynonenal and other reactive aldehydes to alcohols, which are probably less toxic, could play a role in the general defence system of the liver against toxic products arising from radical-induced lipid peroxidation.
The mechanism of action of 4-hydroxynonenal in cell injury.
Uptake of secondary autoxidation products of linoleic acid by the rat
Incorporation of secondary autoxidation products (SP) of linoleic acid into the rat body was investigated. Radioactive SP was administered orally to a group of 5 rats, and excretions of radioactive
Acetaminophen-induced hepatic necrosis. I. Role of drug metabolism.
It is proposed thatacetaminophen-induced hepatic necrosis is mediated by a toxic metabolite of acetaminophen, which inhibits synthesis of cytochrome P-450 and thereby prevented the hepatic damage.