Damage organelles

Kowald, A. and Kirkwood, T. B. L. Accumulation of defective mitochondria through delayed degradation of damaged organelles and its possible role in the ageing of post-mitotic and dividing cells. Journal of Theoretical Biology 202 145-160 2000. 

Peroxidation damages organelle and cellular membranes, reducing their structural integrity and control of selective absorption aixl active transport... 

It is possible to observe effects of organotin(lV) compounds exposure such as inhibition of cleavage of fertilized eggs, interference with the formation of the mitotic spindle, damages affecting chromosome structure, and electron-dense precipitate formation in organelles. 

To correlate embryonic arrests with the metabolic pathways, and especially to understand why cellular organelles first undergo chemical damages, biological investigations include evaluation of DNA, RNA, protein, glucose, lipid, and adenosine-5 -triphosphate (ATP) contents, whose fractions are extracted and isolated by modified Schneider methods. In particular,... 

In both plant (e.g. [57]) and animal (e.g. [86]) cell systems, cellular respiration has been shown to be a more sensitive indicator of system response to hydro-dynamic stress than membrane integrity, suggesting that intracellular enzymes and/or organelles may be affected at stress levels lower than those required to cause membrane damage. 

In bacteria (Escherichia coli), paraquat is concentrated, reduced to the monocation radical, and combines with molecular oxygen to produce the superoxide radical within the cell. Copper and iron are essential mediators in bactericidal effects. The cytoplasmic membrane is the target organelle in paraquat toxicity to E. coli, and extent of damage correlates positively with levels of these metals (Kohen and Chevion 1988). 

Kohen, R. and M. Chevion. 1988. Cytoplasmic membrane is the target organelle for transition metal mediated damage induced by paraquat in Escherichia coli. Biochemistry 27 2597-2603. 

Liver necrosis is another concern following hexachloroethane exposure. Hexachloroethane is metabolized in the centrilobular area of the liver by way of the microsomal mixed function oxidase system. The relatively nonpolar pentachloroethyl free radical is an intermediate in this pathway. The reaction of the free radical with unsaturated lipids in the cellular or organelle membranes could contribute to hepatocyte damage and necrosis. 

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