Induction of lipid peroxidation in tissues of thallous malonate-treated hamster.

  title={Induction of lipid peroxidation in tissues of thallous malonate-treated hamster.},
  author={H Aoyama and M. Yoshida and Yukio Yamamura},
  volume={53 1},
Toxicity of thallium on isolated rat liver mitochondria: The role of oxidative stress and MPT pore opening
The data strongly supported that the thallium(I)‐induced liver toxicity is a result of the disruptive effect of this metal on the mitochondrial respiratory complexes (I, II, and IV), which are the obvious causes of metal‐induced ROS formation and ATP depletion.
In vitro Interactions of Thallium with Components of the Glutathione-dependent Antioxidant Defence System
The present results show that Tl interacts with all the components of GSH/GSSG antioxidant defence system, and Alterations of this protective pathway could be partially responsible for the oxidative stress associated with Tl toxicity.
Endogenous thiols enhance thallium toxicity
Results indicate that L-met and L-cys administered alone or in combination with PB should not be considered suitable treatments against acute Tl toxic effects because this strategy failed to prevent mortality and Tl accumulation in brain.
Vitamin E and C in the prevention of metal nephrotoxicity in developing rats.
  • D. Appenroth, K. Winnefeld
  • Biology, Medicine
    Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie
  • 1998
A comparison of hepatocyte cytotoxic mechanisms for thallium (I) and thallium (III)
Both Tl (I) and Tl(III) cytotoxicities were associated with mutual mitochondrial/lysosomal injuries (cross‐talk) initiated by increased ROS formation resulted from metal‐CYP2E1 destructive interaction or metal‐induced disruption of mitochondrial electron transfer chain.
Study of acute biochemical effects of thallium toxicity in mouse urine by NMR spectroscopy
The present study indicates the great potential of NMR‐based metabonomics in mapping metabolic response for toxicology, which could ultimately lead to identification of potential markers for Tl toxicity.
Delayed effects of thallium in the rat brain: regional changes in lipid peroxidation and behavioral markers, but moderate alterations in antioxidants, after a single administration.
Oxidative stress and DNA damage in broad bean (Vicia faba L.) seedlings induced by thallium
Results obtained indicate that oxidative stress is involved in the mechanism of Tl toxicity and that the tolerance of broad bean to Tl is achieved, at least in part, through the increased activity of antioxidant enzymes.
Thallium(I) and thallium(III) induce apoptosis in isolated rat hepatocytes by alterations in mitochondrial function and generation of ROS
Environmental metal toxins, generated through diverse anthropogenic activities, constitute one of the major contaminants that have led to global dispersion of these toxic metals in the ecosystem.


Induction of lipid peroxidation in rats by mercuric chloride.
Twenty-four hr after the subcutaneous injection of 0.015 mmol of mercuric chloride/kg/day into male rats for 2 days, the rats exhibited biochemical alterations in the kidneys, including diene
Cellular toxicity and lipid peroxidation in response to mercury.
  • A. Tappel
  • Chemistry, Biology
    Annals of the New York Academy of Sciences
  • 1980
These examples show that practical information on interactions involving in vivo lipid peroxidation can be obtained by studies that use the pentane method.
Bromobenzene-induced liver necrosis. Protective role of glutathione and evidence for 3,4-bromobenzene oxide as the hepatotoxic metabolite.
A dose threshold exists for bromobenzene-induced hepatic necrosis and it is demonstrated that the hepatotoxic metabolite is preferentially conjugated (detoxified) with glutathione, thereby depleting glutATHione from the liver.
Thallium Induced Changes in Behavioral Patterns: Correlation With Altered Lipid Peroxidation and Lysosomal Enzyme Activity in Brain Regions of Male Rats
The study suggests that the target regions of thallium in the brain include the cortex, the cerebellum and the brainstem, and the dose-response relationships, found for certain pairs of behavioral acts, were correlated with biochemical changes in one or more brain regions.
Glutathione peroxidase activity in selenium-deficient rat liver.
  • R. Lawrence, R. Burk
  • Biology, Computer Science
    Biochemical and biophysical research communications
  • 1976
Mechanisms of action of selenium and vitamin E in protection of biological membranes.
Results demonstrate that both selenium and vitamin E are required to protect hepatic mitochondria and microsomes from peroxidative degradation, and support for the "Biological Antioxidant Theory" is largely circumstantial.