Disease relevance of Dark Adaptation

• Of 26 patients hospitalized with mild to moderate alcohol-associated cirrhosis, 14 had dark-adaptation abnormalities consistent with marginal vitamin-A status [1].
• Aland Island eye disease (AIED) is an X-chromosomal disorder characterized by reduced visual acuity, progressive axial myopia, regular astigmatism, latent nystagmus, foveal hypoplasia, defective dark adaptation, and fundus hypopigmentation [2].
• These studies suggest high dose and long term p.o. vitamin A and zinc therapy may be required to correct abnormalities in dark adaptation in patients with primary biliary cirrhosis [3].
• BACKGROUND: Zinc deficiency may result in abnormal dark adaptation or night blindness, a symptom primarily of vitamin A deficiency [4].
• Effect of short-term, high-dose retinol on dark adaptation in aging and early age-related maculopathy [5].

Psychiatry related information on Dark Adaptation

• A lithium-induced strong reduction of foveal dark-adaptation was found in healthy volunteers, and a lithium-induced reduction was also measured in patients with affective psychoses [6].
• Improvement in taste and olfaction correlated with a reversal of serum vitamin A levels and dark adaptation toward normal [7].

High impact information on Dark Adaptation

• Mutations in the gene encoding 11-cis retinol dehydrogenase cause delayed dark adaptation and fundus albipunctatus [8].
• Delayed dark adaptation is likely due to accumulation in discs of the noncovalent complex between opsin and all-trans-RAL [9].
• Bleaching of rhodopsin markedly desensitizes the vertebrate visual system during a subsequent period of dark adaptation [10].
• This indicates a migration of retinoid between the two tissues, the direction of which is dictated by the state of light or dark adaptation of the photoreceptors [11].
• Rhodopsin phosphorylation: from terminating single photon responses to photoreceptor dark adaptation [12].

Chemical compound and disease context of Dark Adaptation

• Overall, Casodex was well tolerated; there were no reports of light/dark adaptation problems or pulmonary fibrosis, and only one case of alcohol intolerance, which was not considered by the investigator to be treatment related [13].
• Thus, the conversion (dehydrogenation) of vitamin A alcohol to vitamin A aldehyde is impaired, with a resulting abnormality in dark adaptation, i.e., night blindness [14].
• Improvement in secondary sexual characteristics, normalization of plasma ammonia and serum testosterone levels, and reversal of dark adaptation abnormality and anergy following zinc supplementation to sickle cell anemia subjects have been observed [15].
• Ocular sicca, decreased dark adaptation and intracranial hypertension are identified as "certain" side effects from isotretinoin and clinicians are provided guidelines for care and follow-up [16].
• In one group of patients being evaluated for possible efficacy of a retinoic acid analogue in treating psoriasis, several patients complained of difficulty driving at night due to decreased dark adaptation which we were able to document [17].

Biological context of Dark Adaptation

• The rapid reduction in chloroplast ATPase activity during dark adaptation was prevented by a phosphopeptide containing the 14-3-3 interaction motif, demonstrating a role for endogenous 14-3-3 in the down-regulation of the CF(o)F(1) activity [18].
• At bleaching levels under which patients suffering from fundus albipunctatus could be detected unequivocally, 11-cis-retinol dehydrogenase knockout animals displayed normal dark adaptation kinetics [19].
• In the case of the monomer, the extent of light adaptation, i.e., the fraction of BR molecules containing 13-cis-retinal as chromophore which is converted by illumination to the respective pigment with the all-trans isomer, is reduced by 50% or more, and the rate of dark adaptation is slowed down about 2.5 times [20].
• Although patients with RP1 mutations had, on average, slightly better visual acuity than patients with rhodopsin mutations, there was no statistically significant difference in final dark-adaptation thresholds, visual field diameters, or cone electroretinogram (ERG) amplitudes [21].
• Phototransduction sensitivity was normal for both lines, and dark-adaptation recovery after bleaching rhodopsin was normal [22].

Anatomical context of Dark Adaptation

• Role of noncovalent binding of 11-cis-retinal to opsin in dark adaptation of rod and cone photoreceptors [23].
• Moreover, dark-adaptation for several days lowers zif268 expression in visual cortex, and expression rapidly returns to control levels upon subsequent light exposure [24].
• It is suggested that the major pathway for rhodopsin regeneration during dark adaptation in the intact eye is transport of 11-cis-retinal from the pigment epithelium to the retina [25].
• We review a large body of evidence showing that the time-course of human dark adaptation and pigment regeneration is determined by the local concentration of 11-cis retinal, and that after a large bleach the recovery is limited by the rate at which 11-cis retinal is delivered to opsin in the bleached rod outer segments [26].
• Then we analyse the time-course of three aspects of human dark adaptation: the recovery of psychophysical threshold, the recovery of rod photoreceptor circulating current, and the regeneration of rhodopsin [26].

Associations of Dark Adaptation with chemical compounds

• Plasma retinol levels were measured at each test of dark adaptation [27].
• Here, we show that the noncovalent interaction between 11-cis-retinal and opsin affects the rate of dark adaptation [23].
• Effect of the synthetic retinoid fenretinide on dark adaptation and the ocular surface [27].
• Benefit of docosahexaenoic acid supplements to dark adaptation in dyslexics [28].
• Vitamin-A supplementation was associated with significant (p less than 0.05-0.005) improvement in dark adaptation and increased plasma concentrations of retinyl esters, retinol, and retinol-binding protein [1].

Gene context of Dark Adaptation

• The photosensitivity of Rlbp1(-/-) mice is normal but rhodopsin regeneration, 11-cis-retinal production, and dark adaptation after illumination are delayed by >10-fold [29].
• Knockdown of cone-specific kinase GRK7 in larval zebrafish leads to impaired cone response recovery and delayed dark adaptation [30].
• In this study, light-activated chloroplast and psbD transcription were studied after dark adaptation of 21-day-old light-grown Arabidopsis plants [31].
• We speculate that evolutionary alterations may increase the retinoid metabolite recycling capacity of ABCA4 and may improve dark adaptation [32].
• The second aim was to determine whether prolonged dark adaptation affects protein expression of two important Cx in retina: neuronal Cx36 and glial Cx43 [33].

Analytical, diagnostic and therapeutic context of Dark Adaptation

• Patients from two families, one with a mutation in codon 167 (Gly167Asp) leading to macular degeneration and another with a mutation in codon 210 (Pro210Ser) leading to retinitis pigmentosa, were studied with clinical examinations and measurements of rod and cone sensitivities and dark adaptation, electroretinography, and rhodopsin levels [34].
• Electrooculography and dark adaptation in patients with affective and schizoaffective psychoses: early physiological effects of carbamazepine and lithium [35].
• The elevated serum melatonin concentration in the control group under dark adaptation at night was suppressed after the series of 10-msec light stimuli used for measurement of ERG [36].
• This includes isopter perimetry, colour discrimination, recovery of sensitivity during dark adaptation and refraction at both far and near points, in order to record night myopia as well as night presbyopia [37].
• Two other commonly used diagnostic tests are: functional testing for nightblindness using dark adaptation time, and pathological testing for ocular signs of conjunctival xerosis, with or without the use of Rose Bengal or lissamine green dye [38].

References