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Effects of roxarsone on pigmentation and coccidiosis in broilers.

Roxarsone (0.005%) medicated chickens inoculated at seven weeks of age with Eimeria maxima oocysts had significantly higher pigment levels in blood plasma than did unmedicated controls. Unmedicated E. maxima infected birds had significantly lower pigment levels compared to uninoculated controls. Uninoculated roxarsone medicated controls showed no increase in pigment levels over uninoculated unmedicated birds. This experimental design demonstrates that the beneficial effect of roxarsone medication is due to anticoccidial action rather than an increase in pigmentation after feeding the yellow-colored roxarsone. Since uninoculated birds gained more rapidly if roxarsone (0.025%) was added to the diet, the drug also appears to stimulate growth as well as to protect against coccidial infection. In two floor-pen experiments roxarsone demonstrated anticoccidial activity as measured by higher pigment scores than unmedicated infected controls. The coccidial infection was induced after seeding the litter with oocysts from birds infected with E. acervulina, E. brunetti, E. hagani, E. maxima, E. mivati, E. necatrix, E. praecox, and E. tenella. Pigmentation levels were significantly higher in plasma and skin of roxarsone medicated chickens in two experiments and in shanks in one experiment. Similar protection against depigmentation was demonstrated by adding roxarsone to feed medicated with nequinate. These results involving addition of roxarsone may explain some equivocal reports on pigmentation, weight gains or feed conversion. Some previous investigators appear to have used an inadequate experimental design by omitting use of unmedicated uninoculated controls or to have made no attempt to monitor for presence or absence of coccidiosis.

Animals↗

Photophysical studies of A2-E, putative precursor of lipofuscin, in human retinal pigment epithelial cells.

With age, human retinal pigment epithelial cells accumulate lipofuscin that can absorb photons in the visible range leading to light-induced damage and impaired vision. A putative precursor of lipofuscin, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E, 5E,7E- octatetraenyl]-1-(2-hydroxyethyl)-4-[4-methyl-6-(2,6,6-trimethyl-1 - cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2-E), has recently been isolated and characterized from aged human retinal pigment epithelial cells. We have found that A2-E inhibits the growth of human retinal pigment epithelial cells at concentrations greater than 1 microM. Time-resolved fluorescence measurements of 1 microM A2-E in solution, performed under 413 nm excitation, showed that fluorescence wave forms integrated across the spectrum (450-600 nm) were best-fitted with three decay times in the nanosecond and subnanosecond time scale: 6.6, 1.9 and 0.33 ns. Untreated retinal pigment epithelial cells were characterized by three fluorescence lifetimes: 6.3, 1.7 and 0.35 ns. In retinal pigment epithelial cells treated with 1 microM A2-E, the fluorescence decay was significantly faster, with the marked presence (approximately equal to 30%) of a fourth short lifetime (0.12 ns). These fluorescence decay times for A2-E bound to human retinal pigment epithelial cells are similar to those of lipofuscin granules isolated from aged human retinal pigment epithelial cells. This similarity supports the hypothesis that A2-E is a precursor of lipofuscin and suggests that A2-E may play a role in the overall light damage associated with age-related retinal diseases.

Aging↗

[Pigmentation and venous stasis].

Local pigmentations can occur in the course of venous diseases and are said to be secondary to venous stasis and due to blood pigment. Most often, the pigment is haemosiderin and more rarely melenin pigments. Haemosiderin is a result of dermal biligenesis of extravasated red blood cells, the erythrodiapedesis being due to alterations in the vessel wall. Melanin pigments remain a mystery. Meaanoid may stimulate dermal melanocytes more than the true melanocytes of neural origin which have migrated to the epidermis. Above all, the problem is dominated by stasis and its microvascular and tissue consequences. The pigmentation is part of the "microangiopathy of stasis", as are the pigmentations occurring after therapeutic sclerosis.

Capillaries↗

Experimental evidence for autonomous action of the periodic albinism (ap) gene within developing retinal pigment cells and melanophores of Xenopus laevis.

Genes which affect pigment elaboration may do so by autonomous action within the developing pigment cells or by way of tissue interactions leading to pigment cell differentiation. The site of action of the periodic albinism (ap) gene was investigated by substituting presumptive neural ectoderm of gastrulae of one genotype with uncommitted ectoderm of different genotype. Retinal pigment cells and melanophores arising from such grafts were found to differentiate according to their own genotype in spite of having spent their entire developmental history in tissues of different genotype. This finding demonstrates autonomous action of the ap gene within pigment cell derivatives and does not support recent proposals that the ap gene is involved in inductive interactions leading to melanogenesis. Experiments in which portions of presumptive dorsal mesoderm, implanted in gastrulae of different genotype, induced secondary pigment cells of host phenotype further support the proposal that the ap effect on pigment cells is not mediated by inductive interactions.

Albinism↗

Posterior corneal pigmentation and fibrous proliferation by iris melanocytes.

Pigmentation of the posterior corneal surface results either from endothelial phagocytosis of free melanin pigment or from the presence of iris melanocytes, iris pigment epithelial cells, or pigment-containing macrophages on the posterior corneal surface. Although this is occasionally seen clinically, it is more often noted at histopathologic evaluation after operative or accidental ocular trauma. Three cases of posterior corneal pigmentation by iris melanocytes are reported. In one case, the pigmented membrane was the major cause of considerable visual impairment and was documented with clinical photographs and specular microscopy. By light and electron microscopy, all three cases were consistent with findings of posterior corneal pigmentation by iris stromal melanocytes that had acquired endothelium-like morphologic characteristics. We also consider the possible contribution of these melanocytes to posterior collagen layers of the cornea.

Aged↗

Successful treatment of treatment-resistant laser-induced pigment darkening of a cosmetic tattoo.

BACKGROUND AND OBJECTIVE: Cosmetic tattoo removal has a reported risk of immediate pigment darkening when treated with a high energy, nanosecond pulsed-laser system. Surgical treatment options for this reaction are limited and carry significant risk of scarring and permanent pigment alterations. This report describes the response of a resistant Q-switched ruby laser-induced cosmetic tattoo ink darkening to multiple treatments with the Q-switched alexandrite laser and Q-switch Nd:YAG laser and textural improvement with the UltraPulse CO(2) laser. STUDY DESIGN/MATERIALS AND METHODS: A woman with Q-switched ruby laser-induced pigment darkening of a cosmetic tattoo of the upper lip resistant to four further treatments with the ruby laser and two chemical peels received a total of 26 treatments with the Q-switched alexandrite and Nd:YAG lasers and a single treatment with the UltraPulse CO(2) laser, most treatments being done at monthly intervals. RESULTS: Treatment of the affected areas with the Q-switched alexandrite and Nd:YAG lasers resulted in complete clearing of the pigment without scarring, but revealed some preexisting textural changes. Use of the UltraPulse CO(2) laser smoothed the surface irregularities. CONCLUSION: The Q-switched pigment lasers are a useful modality for treating this pigment darkening reaction. As in this case, multiple treatment sessions with the laser may be necessary but the pigment can be expected to clear eventually without scarring. Any textural changes may be blended with the UltraPulse CO(2) laser with further improvement.

Adult↗

Comparative analysis of the uptake and expression of plasmid vectors in human ciliary and retinal pigment epithelial cells in vitro.

The retinal pigment epithelium is uniquely suited to gene therapy that uses lipid-mediated DNA transfer due to its high phagocytic activity in situ. We compared the relative efficacy of phagocytosis on the uptake of labeled plasmid vectors by retinal pigment epithelial and ciliary epithelial cells in vitro. Relative levels of endocytosis were then compared with the efficiency of marker transgene expression in these cells. Human retinal pigment epithelial and ciliary epithelial cells from a single donor were isolated and expanded in vitro. Polyplex-mediated transfections were performed using a rhodamine-labeled expression vector for green fluorescent protein. Rhodamine-labeled endosomes were examined by fluorescence microscopy at different time points. Rhodamine labeling and green fluorescent protein expression were analyzed by flow cytometry 48 h after transfection. These gene transfer studies showed that expression of transgenes does occur in both human retinal pigment epithelial and ciliary epithelial cells in vitro. Endocytosis of labeled plasmid vectors occurs at a significantly higher number and density in retinal pigment epithelial cells than in ciliary epithelial cells (P < 0.04). However, the efficiency of marker transgene expression is similar in the two cell types. These studies demonstrate that the higher intrinsic phagocytic activity does not enhance the efficacy of transgene expression in retinal pigment epithelial cells in vitro. Both human retinal pigment epithelial and ciliary epithelial cells are competent recipients for lipid-mediated gene transfer, and transgene expression occurs at similar levels in both cell types.

Animals↗

Quail melanoblast migration in two breeds of fowl and in their hybrids: evidence for a dominant genic control of the mesodermal pigment cell pattern through the tissue environment.

In the Silkie fowl large numbers of melanocytes invade most internal tissues and organs. The factors involved in this internal pigment cell pattern were studied by grafting quail neural tube segments into White Leghorn, White Silkie, and F1 hybrids (White Silkie male X White Leghorn female). Sections of quail neural tube five somites long, excised at the level of the last formed somites, were grafted isotopically and ischoronically. Various tissues and organs (mesenteries, muscles, testis, ovary, mesonephros, metanephros, and adrenals) excised from the internal region corresponding to the peripheral transverse strip of quail melanocytes, were studied after staining by the Feulgen-Rossenbeck technique. Despite some variations in pigment cell density, Silkie and hybrid grafted embryos exhibited an extensive quail internal pigmentation similar to the melanocyte distribution in the Silkie breed. In white Leghorn host embryos, the internal pigmentation remained limited. These results show the part played by tissular factors in the expression of the Silkie pigment phenotype and that this genetic tissular character is dominant. On the contrary, White Leghorn embryos, grafted with Silkie neural tube segments, never exhibited any internal pigmentation; the melanocytes deriving from the grafted Silkie neural tube were only localized at the dermoepidermal level. Thus, the migrating and/or differentiating capabilities of the Silkie premelanoblasts are different from those of quail premelanoblasts. The sex-linked inhibitor of the White Leghorn tissue interferes at the level of the pigment cells of chickens but not of quails.

Animals↗

Treatment of recalcitrant-pigmented flat warts using frequency-doubled Q-switched Nd-YAG laser.

BACKGROUND AND OBJECTIVE: Recalcitrant-pigmented flat warts may persist for years despite treatment. Many methods have been used to manage pigmented flat warts, but their efficiencies are varied. Since pigmented flat warts are very similar to lentigo clinically, we used frequency-doubled Q-switched (FDQS) Nd-YAG laser at the wavelength of 532 nm to treat recalcitrant-pigmented flat warts and evaluated the effect. STUDY DESIGN/MATERIALS AND METHODS: Seven patients with recalcitrant-pigmented flat warts were enrolled in this study. We set the FDQS Nd-YAG laser to deliver 2.5 J/cm(2) fluence at the wavelength of 532 nm to treat these lesions. After 6 months, we evaluated the recurrence of pigmented flat warts, pigmentary, and textural changes on the treated areas. RESULTS: There were absences of recurrent lesions, pigmentary, and textural changes on the treated areas of these seven patients after 6 months. CONCLUSIONS: Through both selective photothermolysis effect and propagation of photoacoustic waves, FDQS Nd-YAG laser at the wavelength of 532 nm can be used as an effective alternative to treat recalcitrant pigmented flat warts.

Adolescent↗

Tea pigments inhibit the production of type 1 (T(H1)) and type 2 (T(H2)) helper T cell cytokines in CD4(+) T cells.

Tea pigments are oxidized products of polyphenols derived from tea leaves (Camellia sinensis). Theaflavins are constituents of tea pigments with antioxidant, antineoplastic and antiinflammatory properties similar to their parent compounds. The biological properties of polyphenols and theaflavins have been linked to their capacity to inhibit the activation of nuclear factor-kappaB (NF-kappaB), a transcription factor, which is critically involved in the molecular regulation of a number of proinflammatory cytokines. The current study examines the requirement for NF-kappaB in the immunosuppressive effects mediated by tea antioxidants. Specifically, we tested the hypothesis that cytokines produced by type 1 (T(H1)) CD4(+) T cells which require NF-kappaB for gene expression, such as interleukin-2 (IL-2) and interferon gamma (IFN gamma), are selectively inhibited by tea pigments. We found that tea pigments potently suppress IL-2 secretion, IL-2 gene expression and the activation of NF-kappaB in murine spleens enriched for CD4(+) T cells, as expected. Consistent with our hypothesis, tea pigments also inhibited the induction of IFNgamma mRNA. However, the expression of the T(H2) cytokines IL-4 and IL-5, which lack functional NF-kappaB sites within their promoters was unexpectedly suppressed by tea pigments, as well. The results indicate that NF-kappaB may be only one of multiple transcription factors inhibited by tea pigments.

Animals↗

The BMP/CHORDIN antagonism controls sensory pigment cell specification and differentiation in the ascidian embryo.

We have investigated the role of the bone morphogenetic protein (BMP) pathway during neural tissue formation in the ascidian embryo. The orthologue of the BMP antagonist, chordin, was isolated from the ascidian Halocynthia roretzi. While both the expression pattern and the phenotype observed by overexpressing chordin or BMPb (the dpp-subclass BMP) do not suggest a role for these factors in neural induction, BMP/CHORDIN antagonism was found to affect neural patterning. Overexpression of BMPb induced ectopic sensory pigment cells in the brain lineages that do not normally form pigment cells and suppressed pressure organ formation within the brain. Reciprocally, overexpressing chordin suppressed pigment cell formation and induced ectopic pressure organ. We show that pigment cell formation occurs in three steps. (1) During cleavage stages ectodermal cells are neuralized by a vegetal signal that can be substituted by bFGF. (2) At the early gastrula stage, BMPb secreted from the lateral nerve cord blastomeres induces those neuralized blastomeres in close proximity to adopt a pigment cell fate. (3) At the tailbud stage, among these pigment cell precursors, BMPb induces the differentiation of specifically the anterior type of pigment cell, the otolith; while posteriorly, CHORDIN suppresses BMP activity and allows ocellus differentiation.

Animals↗

A one year study of the macular pigment: the effect of 140 days of a lutein supplement.

A low density of macular pigment may represent a risk factor for age-related macular degeneration (AMD) by permitting greater blue light damage. This study was carried out to determine the effects on macular pigment optical density of dietary supplementation with lutein, one of the pigment constituents. Two subjects consumed lutein esters, equivalent to 30 mg of free lutein per day, for a period of 140 days. Macular pigment optical density was determined by heterochromatic flicker photometry before, during, and after the supplementation period. Serum lutein concentration was also obtained through the analysis of blood samples by high-performance liquid chromatography. Twenty to 40 days after the subjects commenced taking the lutein supplement, their macular pigment optical density began to increase uniformly at an average rate of 1.13+/-0.12 milliabsorbance units/day. During this same period, the serum concentration of lutein increased roughly tenfold, approaching a steady state plateau. The optical density curve eventually levelled off 40 to 50 days after the subjects discontinued the supplement. During the same 40 to 50 days, the serum concentration returned to baseline. Thereafter, little or no decrease in optical density was observed. The mean increases in the macular pigment optical density were 39% and 21% in the eyes of the two subjects respectively. In conclusion, the modest period of supplementation has been estimated to have produced in the subjects a 30 to 40% reduction in blue light reaching the photoreceptors, Bruch's membrane, and the retinal pigment epithelium, the vulnerable tissues affected by AMD.

Adult↗

Two spectral types of retinal light damage occur in albino as well as in pigmented rat: no essential role for melanin.

Earlier we showed that two spectral types of retinal damage occur in the pigmented rat. In the present study we investigated whether the same is true for albino rats. When investigating this issue we implicitly investigated the role of melanin in both damage types. An albinotic (Wistar) and a pigmented (Long Evans) strain of rats were used. Under anesthesia, a small part of the retina was irradiated at either 380 nm or at 470 nm. Three days later, the retina was analysed by funduscopy and prepared for light microscopy. Funduscopy showed no signs of damage in the albinotic retina. In the pigmented retina a decoloration of the fundus was noticed after irradiations starting from retinal doses of 0.6+/-0.1 J cm-2 at 380 nm, and from 489+/-71 J cm-2 at 470 nm. By light microscopy, retinal damage was found in the albino retina. The histologic manifestations at 380 nm differed from those at 470 nm. Irradiation at 380 nm at a dose of 0. 5-0.9 J cm-2 damaged a few scattered photoreceptor cells. At doses of 1.2-1.6 J cm-2 all rods were damaged, while the other retinal layers showed no changes. These findings were similar to those found at 380 nm in the pigmented rat. At 470 nm, damage was found most prominently in the retinal pigment epithelium. These cells showed swelling and an increased number of dark inclusions. Threshold damage occurred at doses of 250-500 J cm-2. Again, the pathology in the pigmented rat was highly similar to that in the albino rat. The results show that both spectral damage types occur in albino as well as in pigmented retina. Therefore, melanin plays no crucial role in these light damage types.

Albinism, Ocular↗

Verapamil inhibits proliferation, migration and protein kinase C activity in human retinal pigment epithelial cells.

The effects of three calcium channel blockers, verapamil, diltiazem and nifedipine, were examined on in vitro proliferation and migration of human retinal pigment epithelial cells. Human retinal pigment epithelial cells were seeded in Dulbecco's modified essential medium with 10% fetal bovine serum and different concentrations of the three calcium channel blockers. After 3 days of treatment, cell proliferation was determined by cell counting and by [3H]-thymidine uptake. Cell viability was determined with trypan blue exclusion. For determination of cell migration, retinal pigment epithelial cells were grown to confluence and then growth-inhibited with mitomycin C. After a 3 mm zone was denuded, the cells were treated with different concentrations of the calcium channel antagonists. After 24 hr, the cells that had migrated over the wound edge were counted. To determine the involvement of protein kinase C in the verapamil effect, its activity was measured in both verapamil-treated and untreated cells. Verapamil dose dependently inhibited serum-induced proliferation of retinal pigment epithelial cells, when measured by cell number (IC50 14.6 microM) or [3H]-thymidine incorporation (IC50 11.3 microM). At concentrations of 15 microM and below, there was no effect on cell viability, as determined by morphology and trypan blue exclusion. Diltiazem inhibited cell proliferation at a concentration of 100 microM; however, 100 microM nifedipine had no effect. Verapamil showed a significant inhibition of serum-induced migration in the range of 10 microM to 0.1 microM. The IC50 of the inhibition of retinal pigment epithelial cell proliferation and migration by verapamil is significantly higher than that seen for effects on calcium channel blockage. Eight micromolar verapamil reversibly inhibited total protein kinase-C activity in retinal pigment epithelial cells suggesting the possibility that the drug may act by inhibiting the protein kinase-C pathway. These data suggest the potential of the calcium channel blocker verapamil as a pharmacological modulator of disorders such as proliferative vitreoretinopathy in which there is increased retinal pigment epithelial cell proliferation and migration.

Calcium Channel Blockers↗

Patterned anomalies of the retinal pigment epithelium: dystrophy or syndrome?

Under the heading of patterned dystrophies of the central pigment epithelium have been included, in some recent publications, the reticular and macroreticular dystrophies described respectively by Sjögren and Mesker et al. (both probably autosomal recessive hereditary conditions) as well as Deutman's butterfly-shaped dystrophy and fundus pulverulentus (both with autosomal dominant heredity), occurring in a few families. We have recently seen 6 patients with patterned anomalies of the central retinal pigment epithelium. The cause of this pigment anomaly was different in each case: Stargardt's macular degeneration associated with fundus flavimaculatus, drusen of Bruch's membrane, choroidal folds, adult (non-hereditary) vitelliform degeneration, bull's eye degeneration of the macula in chronic rheumatoid arthritis, and detachment of the pigment epithelium. In only one case, that of Stargardt's degeneration, was the condition hereditary (autosomal recessive) so that the term dystrophy (= hereditary degeneration) would be justified; all the other cases were non-hereditary conditions. The central retinal pigment epithelium can only react in a limited number of ways to pathological stimuli: one way is the patterned distribution of pigment. This argues against the concept of patterned dystrophy of the retinal pigment epithelium, especially as under this heading conditions with different hereditary characteristics are lumped together.

Adult↗

Different effects of 1-methyl-4-phenyl-pyridinium (MPP+) on monoamine oxidase of dopaminergic terminals in caudate nucleus slices from pigmented and from albino rabbits.

Slices of caudate nucleus from pigmented and from albino rabbits were preincubated in vitro for 24 h with different concentrations of the neurotoxic compound MPP+. Subsequently, endogenous dopamine (DA) in the slices was determined by HPLC. MPP+ (1 and 3.2 mumol/l) was more effective in diminishing DA levels in caudate nucleus slices from albino than in slices from pigmented rabbits. Following 24 h pretreatment with MPP+, the accumulation of [3H]-DA in caudate nucleus slices from pigmented rabbits was either enhanced (at 0.32 mumol/l, 1 mumol/l and 3.2 mumol/l MPP+) or reduced (at 32 mumol/l MPP+). In contrast, MPP+ did not enhance the accumulation of [3H]-DA in caudate nucleus tissue from albino rabbits and was more potent in reducing the [3H]-DA content in slices from albino than in slices from pigmented rabbits. When the selective type A monoamine oxidase (MAO) inhibitor clorgyline was present during pre-incubation, but not when the selective type B MAO inhibitor deprenyl was, the concentration-response curve for MPP+ with caudate nucleus slices from pigmented rabbits was similar to that obtained with slices from albino rabbits. Clorgyline and deprenyl did not change the effects of MPP+ in caudate nucleus slices from albino rabbits. These findings are compatible with the hypothesis that the MAO within dopaminergic terminals in the caudate nucleus of pigmented, but not of albino, rabbits is of type A since MAO-A is preferentially inhibited by MPP+. In line with this hypothesis, the accumulation of the preferential MAO-A substrate [3H]-5-HT in caudate nucleus slices from pigmented rabbits was about 39% lower than that in slices from albino rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-4-phenylpyridinium↗

The microtubular system of crayfish retinula cells and its changes in relation to screening-pigment migration.

The organization of the microtubular system in crayfish retinula cells and its changes in relation to the light-dependent migrations of the screening pigment were studied by electron microscopy. A massive column of microtubules extends longitudinally throughout each retinula cell and its axon. The column is formed by overlapping fascicles of microtubules that originate from the vicinity of the rhabdomeres at multiple levels along the rhabdom. The pigment granules and other organelles are in general aligned with these fascicles and peripheral to the microtubular column. Close associations between microtubules and pigment granules are frequent. The total number of microtubules decreases nucleofugally from an average of about 500 at the middle of the rhabdom, to 390 at the proximal end of the rhabdom, and 240 in the axon below the basement membrane. The longitudinal distribution of microtubules was found similar for cells with the screening pigment in opposite extreme positions. In cells with the pigment in an intermediate position the number of microtubules was found to be nearly doubled in each of the mentioned levels; however, this change was correlated with a parallel increase in the cross-sectional area of the cells during the intermediate state. Thus, the density of microtubules tends to remain fairly constant throughout the light/dark adaptation cycle. These observations suggest that the microtubular system of the crayfish retinula cells constitutes a relatively stationary framework during screening-pigment movements, and could possibly act as a supportive guiding track for pigment transport.

Animals↗

Modification of spectral sensitivities by screening pigments in the compound eyes of twilight-active fireflies (Coleoptera: Lampyridae).

1. ERG S(lambda) were determined in dark-adapted intact preparations of 6 North American firefly species (Photinus collustrans, marginellus, pyralis, macdermotti, scintillans and Bicellonycha wickershamorum) which restrict their flashing activity to twilight hours. The curves possess narrow (1/2 bandwidth = 50-60 nm) peaks in the yellow (560-580 nm) and a shoulder in the violet (370-420 nm), with a marked attenuation (1.4-2.2 log units) of sensitivity in the green (480-530 nm) region of the spectrum (Fig. 1). Two additional species (Photuris potomaca and frontalis) which initiate flashing at twilight and continue on late into the night (twi-night) possess broad sensitivity maxima around 560 nm (Fig. 3). 2. Selective adaptation experiments isolated near-UV and yellow in P. scintillans (Fig. 2). In the dorsal frontal region of the compound eyes in P. frontalis, high sensitivity existed only in the short wavelength region (near-UV and blue) with a maximum in the blue (lambda max 435 nm) (Fig. 4). 3. The in situ MSP absorption spectrum of the screening pigments was determined in preparations of firefly retina. a) Two kinds of dark brown granules were found in the clear zone region. These granules absorb all across the spectrum with a gradual increase in optical density in the shorter wavelength region in P. pyralis (Fig. 5). b) Besides dark granules, pink-to-red colored screening pigments were present in the vicinity of the rhabdoms. The absorption spectra of these pigments determined in five species were narrow (1/2 bandwidth = 50-80 nm) with species-specific differences in their peak absorption in the green at 525 nm, 510 nm, 512 nm and 517 nm in P. scintillans, macdermotti, collustrans and pyralis, respectively (Fig. 6). A similar pigment was found in P. marginellus with a lambda max at 512 nm (Fig. 7). In all cases, transmission increased both at long and short wavelengths, but more sharply in the long wavelength region (Figs. 6 and 7). Hence each twilight-restricted species has its own unique colored screening pigment. A yellow pigment whose absorption spectrum differed from those found in genus Photinus was found in twi-night active Photuris potomaca (lambda max 461 nm) and night-active P. versicolor (lambda max 456 nm). The transmission of the Photuris pigment increased sharply only in the long wave-length region (Fig. 8).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗