Membrane injury

Figura 4. Membrane injury in leaves of Arabidopsis thaliana L. plants exposed to Cd, and Pb" ions in hydroponics culture for 29 days. Data are mean of 5 replications expressed as % of injury recorded in control.

Chronic injury results primarily from secondary reactions involving membrane injury. The oxidants could cause the formation of free radicals or other, more stable oxidants (such as hydrogen peroxide), which in turn could cause secondary reactions. These secondary reactions could stimulate the production of cellular ethylene, with tissue senescence re suiting. These secondary reactions may predispose plants to increased injury from later acute exposures by limiting their repair capability. This predisposition concept has been noted in several reports. 

Protein, DNA and membrane injury, oxidative stress Phase 11 enzyme induction, inflammation, mitochondrial perturbation ... 

Yatvin MB, Wood PG, Brown SM (1972),Repair of plasma membrane injury and DNA single strand breaks in y-irradiated Escherichia coli B/r and Bs.i. Biochim Biophys Acta 287 390-403 Yatvin MB, Gipp JJ, Dennis WH (1979) Influence of unsaturated fatty acids, membrane fluidity and oxygenation on the survival of an E. coli fatty acid auxotroph following y-irradiation. Int J Radiat Biol 35 539-548... 

Sepe, S. M., and Clark, R. A., Oxidant membrane injury by the neutrophil myeloperoxidase system. II. Injury by stimulated neutrophils and protection by lipid-soluble antioxidants. J. 

The nervous system is also affected in deficiency, with the development of central nervous system necrosis (nutritional encephalomacia), a condition that can be exacerbated by feeding a diet especially rich in polyunsaturated fatty acids. There is also axonal dystrophy in animals maintained for prolonged periods of time on vitamin E-deficient diets. Synthetic antioxidants, but not selenium, can prevent these changes. The neuropathy begins from axonal membrane injury, and then develops as a distal and dying-back type of axonopathy. 

The toxie effeets of T-2 toxin and DAS are similar irre-speetive of route of exposure and species, with ingestion, parenteral administration, and inhalation resulting in lymphoid necrosis, hematotoxicity, and gastrointestinal toxicity (Table 26.2, Figures 26.2 and 26.3). Shock secondary to cardiovascular collapse occurs at high doses. T-2 toxin and DAS also cause dermal and mucous membrane injury on contact. 

The action on cell components results in inhibition of cellular division (mitosis) with decreased tissue respiration that leads to cell death. It produces eye, airway, and skin and mucous membrane injury that can be fatal. Systemic effects with extensive exposures include bone marrow inhibition with a drop in the white blood cell count and gastrointestinal tract damage. 

Photosynthetic inhibition caused by NOx may be due to competition for NADPH between the processes of nitrite reduction and carbon assimilation in chloroplasts. N02 has been shown to cause swelling of chloroplast membranes (Wellburn et al. 1972). Biochemical and membrane injury may be caused by ammonia produced from N03, if it is not utilized soon after its formation. Plants can metabolize the dissolved NOx through their N02 assimilation pathway ... 

Whenthe precursor of A/9 was cloned in 1987 (13), it immediately became apparent that one of the two proteolytic scissions needed to release A(S must occur within a hydrophobic, putatively membrane-spanning region of APP. As hydrolysis of peptide bonds requires water and as all known proteases had their active sites in aqueous compartments of the cell or extracellularly, it was assumed that at least part of the APP TMD must be transiently exposed outside of the membrane, presumably due to prior membrane injury. The only other possibility raised at the time was that the TMD of APP ended just before or at the y-secretase cleavage site however, this was incompatible with available information about the predicted... 

Layden, T. J., and Boyer, J. L., Taurolithocholate-induced cholestasis Taurocholate, but not dehydrocholate, reverses cholestasis and bile canalicular membrane injury. Ges-troenterology 73, 120-128 (1977). 

Yeong ML, Wakefield SJ, Ford H. Hepatocyte membrane injury and bleb formation following low dose comfrey toxicity in rats. Int J Exp Pathol 1993 74 211-7. 

Protein Release. Biomembranes consist of lipids and proteins. The latter may be subdivided into so-called intrinsic and extrinsic proteins (49). Intrinsic proteins supposedly are integrated into the membrane phase primarily by the hydrophobic interaction with lipids. Extrinsic proteins are attached to the membranes. Ionic interactions are believed to be important in the binding of extrinsic proteins. When these proteins dissociate from the membrane, they may be sufficiently hydrophilic to be soluble in the aqueous phase. When freeze-aggregated thylakoids are sedimented, a number of membrane proteins are found in the supernatant fluid. Among them are catalytic proteins involved in energy conservation and electron transport (42,48). The total amount of proteins released depends on freezing conditions and the solute environment, but may be as much as 5% of the total membrane protein (48). When frozen in the presence of a cryoprotective solute, at a sufficient concentration, thylakoids remain functional and do not release proteins in significant amounts. Protein release thus accompanies membrane injury and, in fact, is an indication of such injury. 

The trypanocidal action of nifurtimox derives from its ability to undergo activation by partial reduction to nitro radical anions. Transfer of electrons from the activated drug then forms superoxide radical anions and other reactive oxygen species. Reaction of free radicals results in lipid peroxidation and membrane injury, enzyme inactivation, and DNA damage. Benznidazole also requires a one-electron transfer that generates nitro anion radicals, leading to cellular damage that kills the parasites. 

Effects of Antioxidants. The most important evidence implicating free radicals in DPE membrane injury is the ability to protect against damage with a known radical scavenger. Compounds with the potential ability to provide limited protection against DPE injury by free radical scavenging and other mechanisms include BHA (butylated hydroxyanisole), BHT (butylated hydroxytoluene), EDU N-[2-(2-oxo-l-imidazolidinyl)-... 

The inhibitory action of cepharanthamine on the release of potassium ions following membrane injury has been studied/ ... 

Yeong, M.L., S.J. Wakefield, and H.C. Ford. 1993. Hepatocyte membrane injury and bleb formahon following low dose cornfrey toxicity in rats. Int. J. Exp. Pathol. 74(2) 211-217. 

Alteration of cell membranes Injury bacterial plasma membranes lead to cell death through leakage of the cell contents and associated disruption of the cross-membrane potential (which essentially are ion concentration gradients). 

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