Cytochrome retinitis

It has been shown in many studies that protective effects of carotenoids can be observed only at small carotenoid concentrations, whereas at high concentrations carotenoids exert pro-oxidant effects via propagation of free radical damage (Chucair et al., 2007 Lowe et al., 1999 Palozza, 1998, 2001 Young and Lowe, 2001). For example, supplementation of rat retinal photoreceptors with small concentrations of lutein and zeaxanthin reduces apoptosis in photoreceptors, preserves mitochondrial potential, and prevents cytochrome c release from mitochondria subjected to oxidative stress induced by paraquat or hydrogen peroxide (Chucair et al., 2007). However, this protective effect has been observed only at low concentrations of xanthophylls, of 0.14 and 0.17 pM for lutein and zeaxanthin, respectively. Higher concentrations of carotenoids have led to deleterious effects (Chucair et al., 2007). 

Proton gradients can be built up in various ways. A very unusual type is represented by bacteriorhodopsin (1), a light-driven proton pump that various bacteria use to produce energy. As with rhodopsin in the eye, the light-sensitive component used here is covalently bound retinal (see p. 358). In photosynthesis (see p. 130), reduced plastoquinone (QH2) transports protons, as well as electrons, through the membrane (Q cycle, 2). The formation of the proton gradient by the respiratory chain is also coupled to redox processes (see p. 140). In complex III, a Q,cycle is responsible for proton translocation (not shown). In cytochrome c oxidase (complex IV, 3), trans-... 

Zhang QY, Raner G, Ding XX, et al. Characterization of the cytochrome P450 CYP2J4-expression in rat small intestine and role in retinoic acid biotransformation from retinal. Arch Biochem Biophys 1998 353 257-264. 

Intoxication may present as inebriation and drowsiness similar to ethanol use. Other symptoms are vomiting, diarrhea, delirium and agitation, back and abdominal pain, and clammy skin. Toxic effects usually follow a latent period of several hours. Formate inhibits mitochondrial cytochromes resulting in neurotoxicity. Ocular signs include blurred vision, dilated pupils, and direct retinal toxicity with optic disc hyperemia and ultimately permanent blindness [91]. Cerebral hemorrhagic necrosis has been reported [92]. Severe poisoning may result in Kussmaul respiration, inspiratory apnea, coma, and death. Urine samples may have the characteristic smell of formaldehyde. An elevated serum osmolal gap from methanol will be evident early in presentation but may disappear after approximately 12 hours. At this time, an elevated anion gap metabolic acidosis from retained formate may be evident. 

Raner, G.M., A.D. Vaz, and M.J. Coon (1996). Metabolism of all-trans, 9-cis, and 13-cis isomers of retinal by purified isozymes of microsomal cytochrome P450 and mechanism-based inhibition... 

The following types of bion ihbrane stacks were investigated by paraciystal-line methods nerve myelin retinal rod outer segment discs human erythrocyte ost membranes sarcoplasmic reticulum chromatophore membrane cytochrome oxidase model membranes photosynthetic membranes. " mitochondrial cristae membranes ... 

The mechanism of ethambutol-induced optic neuropathy is unclear. It has been postulated that it is caused by a disturbance in mitochondrial metabolism. Ethambutol is also a strong chelator of copper, a co-factor of cytochrome c oxidase, which is required for axonal transport in the optic nerves, failure of which, secondary to mitochondrial insufficiency, results in optic neuropathy. Ethambutol is specifically toxic to retinal... 

Numerous biological redox systems have been studied by the spectroelectrochemical approach, including cytochromes, myoglobin, photosynthetic electron transport components, spinach ferrodoxin, blue copper proteins, retinal, and vitamin B 2 analogues. Two classic examples are presented here. 

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