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The clinical and histopathological picture of the pigmented epidermal cyst and the pigmented trichilemmcyst is illustrated by three case-reports. The pigment is melanin, which is located in the epithelium of the cyst-wall, the corneocytes of the lumen and in macrophages in the dermis. The clinical appearance of melanin pigmented cysts is blue due to the Tyndall-phenomenon.
The chicken retina contains rhodopsin (a rod visual pigment) and four kinds of cone visual pigments. The primary structures of chicken red (iodopsin) and rhodopsin have been determined previously. Here we report isolation of three cDNA clones encoding additional pigments from a chicken retinal cDNA library. Based on the partial amino acid sequences of the purified chicken visual pigments together with their biochemical and spectral properties, we have identified these clones as encoding the chicken green, blue, and violet visual pigments. Chicken violet was very similar to human blue not only in absorption maximum (chicken violet, 415 nm; human blue, 419 nm) but also in amino acid sequence (80.6% identical). Interestingly, chicken green was more similar (71-75.1%) than any other known cone pigment (42.0-53.7%) to vertebrate rhodopsins. The fourth additional cone pigment, chicken blue, had relatively low similarity (39.3-54.6%) in amino acid sequence to those of the other vertebrate visual pigments. A phylogenetic tree of vertebrate visual pigments constructed on the basis of amino acid identity indicated that an ancestral visual pigment evolved first into four groups (groups L, S, M1, and M2), each of which includes one of the chicken cone pigments, and that group Rh including vertebrate rhodopsins diverged from group M2 later. Thus, it is suggested that the gene for scotopic vision (rhodopsin) has evolved out of that for photopic vision (cone pigments). The divergence of rhodopsin from cone pigments was accompanied by an increase in negative net charge of the pigment.
BACKGROUND: This study investigated the anti-oxidant properties, starch composition, pasting behavior, structural properties, textural properties and non-targeted metabolomic profiles of pigmented and non-pigmented rice landraces as potential next-generation functional food ingredients. RESULTS: Pigmented rice demonstrated 1.34 times more anti-oxidant activity as compared to non-pigmented rice. Pigmented landraces showcased superior nutritional and functional attributes, including higher total dietary fiber and starch content. Fourier-transform infrared (FTIR) analysis revealed distinct molecular signatures with enhanced peak transmittance, while X-ray diffraction (XRD) indicated greater crystallinity ranging from 36-44.3% in pigmented rice compared with 30-40% in non-pigmented rice, suggesting improved digestibility and processing versatility. Pigmented rice recorded less amylose content hence tended to possess increased adhesiveness values whereas non-pigmented rice revealed greater amylose content hence was coupled with greater hardness values. Field-emission scanning electron microscopy (FE-SEM) images revealed that pigmented rice had densely packed and polygonal starch granules whereas non-pigmented rice had loosely packed starch granules with intergranular voids. Untargeted gas chromatography-mass spectrometry (GC-MS) profiling identified 84 metabolites, including unique compounds such as 3,3-dimethylbutanol and ethanoic acid, along with shared metabolites such as sucrose and linoleic acid, highlighting notable biochemical diversity. Multivariate statistical analyses using principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway mapping further differentiated the metabolomic landscapes, with variable importance in the projection (VIP) scores identifying key bioactive contributors. CONCLUSION: Pigmented rice landraces exhibited significant functional and nutritional advantages, making them promising candidates for functional food development and nutritional improvement programs. These findings support their potential role in advancing sustainable and health-oriented food systems. © 2026 Society of Chemical Industry.
When pigmented and non-pigmented rabbit irides were incubated with various concentrations of 14C-imipramine at equilibrium (120 min), the accumulation of the drug by the pigmented iris was 1.5 times as great as that by the non-pigmented iris. The accumulated drug is lost from both types of irides in a complex fashion. However, even after 120 min of washing, the differences in accumulation remain nearly constant. When accumulation of the drug in the non-pigmented iris was analyzed by discontinuous sucrose density gradient, it was observed that the drug was bound mainly by the low density sucrose fractions where the synaptosomes separate. On the contrary, in the pigmented iris approximately 70% of the drug was found in the melanin-containing fraction. The homogenate from the substantia nigra accumulated 1.5 times more than that from the human brain cortex. The affinity of the drug for bovine iris melanin granules and the synthetic L-dopa melanin was 9.9 X 10(5) M-1 and 3.8 X 10(3) M-1, respectively. On the rabbit iris sphincter muscles, imipramine was evaluated for antimuscarinic effects. The apparent dissociation constants, KB values, for the antagonist in the non-pigmented and pigmented iris were 1.7 X 10(-7) M and 3.8 X 10(-6) M, respectively. The low antimuscarinic activity in the pigmented iris is attributed to the loss of the drug to the pigment. On this basis, relevancy of the drug binding by pigmented tissues to the effects of this tricyclic drug is discussed.
Yellow and white mutants of the strains Nocardia pellegrino SN 5108 R have been isolated. Regarding their morphological and physiological properties, the mutants are identical with the wild type bacteria with the exception of their pigmentation and lipid composition. However, the pigment composition (number, Rf-values and spectra of the pigment components) of the yellow mutant is identical with that of the wild type; as a consequence, the modified pigmentation of the yellow mutant cannot be explained by an altered pigment synthesis. The wild type cells and the mutant SN 5108 G contain three main pigment components designated as I, II and III. Components II and III posses a marked indicator character and show a bathochromic shift in solutions of pH 12 or higher. Components II and III contain functional groups which are able to react with acetic acid yielding acetylated products; after acetylating, no bathochromic shift in alkali occurs. Intact cells of the wild type retain their orange-red pigmentation in buffer solution with a pH-value of 12 or higher. Cells of the yellow mutant, however, change the yellow color immediately after the alkali treatment to orange-red; this new color is identical with that of the wild type and can be changed to yellow by placing the cells into 1 N HCl. Regarding these facts it seems to be very probable that the functional groups of the pigment components II and III are differently bound in the wild type and mutant cells. In the mutant, they are accessible to OH- ions yielding a bathochromic shift while in the wild type cells, OH- ions are unable to provoke this shift. It seems to be also probable that different lipids in the two strains are responsible for the binding of the pigments. So far known, this is the first observation about the occurence of pigment mutants with an altered pigment binding site in the cells.
A yellow autofluorescent pigment, generally thought to be indicative of membrane autoxidation, was found to accumulate in the retinal pigment epithelium (RPE) of rats maintained for 32 weeks on diets producing physiological antioxidant deficiency. The largest build-up of fluorescent pigment occurred in rats fed a diet high in polyunsaturated fatty acids (PUFAs) and deficient in alpha-tocopherol (vitamin E), selenium, sulfur-containing amino acids, and chromium. These latter four nutrients have all been implicated in maintaining the antioxidant status of tissues, whereas PUFAs are pro-oxidants. Dietary supplementation with methionine and chromium significantly reduced the amount of fluorescent pigment accumulated in the RPE. Supplementation with all four nutrients further reduced the amount of fluorescent pigment to a very low level. Rats maintained on a normal laboratory diet, relatively low in PUFAs and presumably adequate in other nutrients, accumulated relatively small amounts of fluorescent pigment in the RPE. Of all tissues in the retina and choroid, the autofluorescent pigment was found to be almost entirely restricted to the RPE. The autofluorescence produced in the RPE by antioxidant deficiency was more concentrated than that produced in the testes, kidney, intestine, and heart. This suggests that the RPE is particularly sensitive to physiological antioxidant deficiencies. The increased fluorescent pigment build-up in the RPE of antioxidant-deficient rats appears to correlate with a decreased RPE melanin content. Similar changes in pigmentation have been reported to occur in human RPE with age and in dominantly inherited retinitis pigmentosa. Thus, with respect to its effect on RPE pigmentation, antioxidant deficiency appears to mimic aging and possibly some aspects of one type of retinitis pigmentosa.
The classification and, therefore, identification of Chromobacterium violaceum has been based upon its ability to produce a violet pigment. Although the organism may yield non-pigmented variants when subcultured on artificial media, the isolation of non-pigmented strains from pathological tissues or from nature had not been reported. With a method established for the identification of C. violaceum regardless of violet pigmentation, non-pigmented strains were isolated from nature. The presence of non-pigmented strains of C. violaceum in nature is of significance to taxonomy and clinical bacteriology. Pigmentation cannot be held as an essential characteristic of the definition of the genus Chromobacterium and gives credence to the suspicion of Sneath (1960, 1966) that the genus is not a natural one. Non-pigmented strains may have been isolated from clinical material but wrongly identified as belonging to other genera of non-pigmented Gram-negative bacilli and regarded as not being pathogenic.
Mixed cultures of melanocytes (M) and keratinocytes (K) are easily obtained from pigmented guinea pig ear skin. They are suitable for the study of pigment transfer from M to K. However, quantitation is difficult because many K are already loaded with pigment prior to cultivation. A technique is presented in which pigment-producing M are co-cultured with K of albino origin. Pigmented guinea pig ear skin is split with trypsin and basal cells including M are harvested. The cell suspension is treated with sodium citrate which prevents the attachment of K (but not of M) to the culture substrate. Ninety per cent pure M cultures are obtained. Five to seven days later, another basal cell suspension is prepared, this time from albino ear skin. This second suspension is seeded on top of the pigment-forming culture of M. The number of contacts between albino K and pigment-forming M increases as a direct function of time. Contrarily, the number of K which become pigmented increases until the fifth day of co-culture and decreases thereafter.
Black to brown amorphous to microcrystalline granules are encountered in histologic sections prepared from tissues fixed in formalin having a low pH. This pigment is produced by acid acting upon hemoglobin and is known as formalin pigment or acid hematin. A similar pigment is also observed in sites of bleeding ulcers in areas of acid production such as the stomach. These pigments exhibit many physical and histochemical properties similiar to pigments produced by some animal parasites as in malaria, schistosoma and pulmonary mites. These parasites disintegrate erythrocytes in an unknown manner, and liberate an acid hematin-like pigment which is phagocytized by the reticuloendothelial system. Since formalin pigment can be considered as an artifact, confusion with other pigments can be avoided by the use of neutral buffered formalin for the fixation of tissues.
Changes in the activity of intracellular and extracellular nuclease of pigment and pigment-free strains of Serratia marcescens were studied. The activity of intra- and extracellular nuclease of the pigment-free strain was higher than that of the pigment strain at all growth stages of the microorganism. The activity of intracellular nuclease in the lag-phase was higher than in the phase of exponential growth of both strains. Prior to cell division the enzyme activity declined in both strains. At the beginning of the stationary phase the activity of intracellular nuclease was relatively stable in both strains. By the end of the stationary phase the activity of intracellular nuclease of the pigment-free strain increased 4--6 fold and that of the pigment strain remained unchanged. Simultaneously the activity of extracellular nuclease of the pigment-free strain increased and that of the pigment strain grew but slightly.
Small fragments of the retinal pigmented epithelium from White Leghorn, Rhode Island Red chick embryos, and from Quail, Starling and Red Partridge embryos, were grafted into the wing bud of White Leghorn chick embryos. Retinal pigmented epithelium of White Leghorn chick embryos did not give rise to pigmentation of feather primordia in the hosts. In contrast, 60% of grafts from Rhode Island Red, Quail, Starling and Red Partridge, gave rise to feather primordia whose pigmentation was identical to that of the donors. Pigmentation depends on the fact that some graft retinal melanocytes diffuse in the wing bud of the host and reach the feather primordia. This was shown by the Feulgen technique in embryos grafted with Quail retinal pigmented epithelium, taking advantage of the fact that Quail cells possess DNA rich nucleoli. The local factors which allow the migration of the melanocytes are probably inactive on the retinal melanocytes of the White Leghorn chick embryos, whose genotype does not contain the "feather pigmentation" character.
In the retina of the frog and certain other animals, melanin pigment granules move in response to light so as to shield photoreceptor outer segments. The granules are contained within the cells of the pigment epithelium (PE) which lie as a continuous sheet between the neural retina and the choroid. Moderate illumination of the eye causes the melanin granules to move from a region within a PE cell body into numerous fingerlike extensions of the cell which interdigitate with the receptor outer segments. This migration takes many minutes and is reversed when the light falling on the eye increases in intensity. Several reviews are concerned with the early descriptions of this phenomenon (6,30) and with more recent experiments (1,5,19). The mechanism of the pigment granule motion is undetermined although there are studies concerning PE ultrastructure (8, 23, 31), scanning electron microscopy of the fingerlike extensions of the PE cells (27), the role of the PE in photoreceptor phagocytosis (32), the nature of the pigment granules (19), and the action spectrum of the light which induces the migration (16). This study reports the presence of a system of microfilaments associated with the pigment granules in the fingerlike extensions processes of the PE cells. We demonstrate by heavy meromyosin (HMM) labeling that the filaments are actinlike in character and suggest that these filaments could be responsible for the migration of the melanin pigment granules.
Histochemical studies were made of pigmented cutaneous lesions from three cases of lepromatous leprosy treated with B663 to determine the nature and histogenesis of the brown pigmentation which develops as a side effect of the drug. One case of DDS-treated leprosy and four cases of untreated leprosy were also investigated histochemically as controls. The brown pigmentation of the skin is due to deposition of a ceroid-like substance in the macrophages, which is a yellowish-brown, acid-fast lipid pigment. It is insoluble in fat solvents and accepts lipid dyes even after lipid extraction by fat solvents. The macrophages in the B663-treated leprosy contain more neutral fat and less phospholipid than the untreated lepromatous leprosy tissues. Ceroid in the macrophages probably originated from unsaturated fatty acids of the leprosy bacilli through oxidation or their binding with the drug. Crystals of the drug were not found in the macrophages in this series, even on the tissues embedded in carbowax or frozen sections.
Besides carotenoids a complex of flexirubin-type pigments was isolated from the gliding bacterium Cytophaga johnsonae Cy jl and separated into 6 components, which partly containe chlorine. In spite of the fact that these components still consist of pigment mixtures, the gross structures of 18 new flexirubin-type pigments could be deduced by spectroscopic and chemical investigations. The results open insights into biosynthesis and structural variety of the flexirubins, the novel non-isoprenoid pigments recently found in Flexibacter elegans.
The pigmented eyes of non albino rats (PVG) accumulated ephedrine, norephedrine and amphetamine. After 15 min accumulation of ephedrine and amphetamine was larger than of norephedrine. Autoradiographic studies showed that accumulation occurred in melanin containing iris and choroid and also in lacrymal glands which lack melanin. Accumulation of tyramine did not occur in eyes containing melanin. The non pigmented eyes of albino rats did not accumulate ephedrine, amphetamine, norephedrine and tyramine. It appeared that in pigmented eyes melanin was a site of loss of ephedrine, amphetamine and norephedrine; hence a smaller amount of drug will be available for interaction with adrenergic neurons and a smaller mydriatic effect will occur. Accumulation is possible only when metabolism is low, as observed with alpha-methylated amines. The four sympathomimetic amines used did not accumulate in the pigmented skin of black and white rats.
Four melanin pigment-containing intracranial tumors were found in three Long-Evans rats in the course of experimental oncogenesis by transplacental ethylnitrosourea (ENU). One of them was a leptomeningeal melanoma. Aside from the presence of scattered melanin-pigmented cells, the other three had the typical histological features of ENU-induced malignant nerve sheath tumors. Two of the three tumors were studied by electron microscopy and in tissue and organ culture systems. One of them demonstrated progressive melanogenesis in vitro; the other failed to produce more melanin and showed increasing differentiation, with a Schwannoma-like pattern by light microscopy. Melanosomes and premelanosomes were identified in both tumors by electron microscopy; the other fine structural features were those of malignant Schwannomas. These observations are relevant to the controversy on the histogenesis of pigmented nerve sheath tumors occasionally encountered in man and on the relationship of these tumors to pigmented nevi. The findings in the present study support the view of Masson that neoplastic nerve sheath cells are capable of melanogenesis.
Pigmented epidermotropic breast carcinoma has to be included in the differential diagnosis of pigmented lesions of the breast. Two rare cases of pigmented Paget's disease and pigmented metastatic breast carcinoma are presented, which mimicked malignant melanoma in both clinical and histological criteria.
The iris anlage of 2-10 and 15 days old chicken embryos were studied histochemically, and by both light and electron microscopy. Light microscopic serial sections showed that pigmentation began at the outer layer of the posterior eye pole and progressed from there forwards to the optic cup margin. The entire outer layer of the optic cup as well as the pupillary margin were completely pigmented by the 4th day of incubation. By the 10th day the posterior iris epithelium was totally pigmented. Electron microscopical studies showed that the first premelanosomes appeared at about the 3rd day of incubation in the anterior iris anlage with the exception of the pupillary margin. It could be shown that melanogenesis progressed through the following steps: premelanosomes, followed by tyrosinase activity in a Golgi-associated system of smooth endoplasmic reticulum (GERL) and small vesicles and finally differentiation of the melanosomes. The possible origin of the premelanosomes and the formation of melanin are discussed.