Extracellular Melanin Research Articles

Fungal melanins and their interactions with metals

Fungal melanins are dark brown or black pigments located in cell walls. They also exist as extracellular polymers. Melanized fungi possess increased virulence and resistance to microbial attack as well as enhanced survival while under environmental stress. Melanins contain various functional groups which provide an array of multiple nonequivalent binding sites for metal ions. Pigmented Cladosporium cladosporoides was shown to biosorb 2.5- to four-fold more Ni, Cu, Zn, Cd, and Pb than albino Penicillium digitatum and at four- to six-fold higher rates. Metal desorption was significantly lower for extracellular melanin than from pigmented or albino biomass which indicated the strength of the melanin-metal bond. At equilibrium, tributyltin chloride (TBTC) concentrations of 2.5 m m, pigmented and albino Aureobasidium pullulans absorbed approximately 0.9 and 0.7 μmol TBTC mg −1 dry wt, respectively, whereas purified extracellular melanin exhibited uptake levels of approximately 22 μmol TBTC mg −1 dry wt at an equilibrium concentration of only 0.4 m m. Addition of melanin to the growth medium reduced the toxic effect of CuSO 4 and TBTC due to melanin metal binding and sequestration.

Insect immunity: early events in the encapsulation process of parasitoid (Leptopilina boulardi) eggs in resistant and susceptible strains of Drosophila.

Eggs of an immune suppressive strain (= virulent) of the parasitoid Leptopilina boulardi are encapsulated neither in resistant nor in susceptible strains of Drosophila melanogaster but are encapsulated in Drosophila yakuba. Eggs of a nonimmune suppressive strain (= avirulent) of the same parasitoid are encapsulated in a resistant strain of D. melanogaster and in D. yakuba but are not encapsulated in a susceptible strain of D. melanogaster. Egg chorion in the 2 parasitoid strains showed the same morphology and the same modifications after egg laying whatever the host strain. When a capsule is built, a small dotted dense layer was first spread on the chorion, followed by accumulation layers of cells (plasmatocytes and lamellocytes) and lastly necrosis of the inner haemocytes. The encapsulated eggs darken only at the time of necrosis of haemocytes. In susceptible hosts, neither the tiny dense layer nor haemocyte accumulation occurred. We concluded that (1) this tiny dense layer was present before the deposition of the first haemocytes, (2) inhibition of deposition of this dense layer was the initial event of the induced immunosuppression, (3) haemocytes other than lamellocytes were engaged in capsule formation, (4) the immunosuppressive factors did not target only the lamellocytes but also the plasmatocytes, (5) darkening of the encapsulated eggs was due to cell necrosis rather than to extracellular melanin deposition.

Ineffective treatment of refractory melasma and postinflammatory hyperpigmentation by Q-switched ruby laser.

Melasma and postinflammatory pigmentation are cosmetic problems with limited options for treatment. To determine whether selective photothermolysis of pigmented cells by Q-switched ruby laser treatment would produce clinical benefit in these disorders. Eight subjects with melasma or postinflammatory hyperpigmentation refractory to traditional treatments were treated with Q-switched ruby laser pulses (694 nm, 40 nanoseconds) at fluences of 15-7.5 J/cm2, and followed. Histology was obtained before and after treatment. Regardless of fluence, no permanent improvement and, in some cases, darkening was seen in each type of lesion. Except for small depression at high fluences in black patients, there were no textural changes after healing. Immediately after treatment, there was epidermal and dermal injury, with extracellular melanin. Several months later, epidermal pigmentation had returned to baseline and dermal macrophages were apparently focally increased. The Q-switched ruby laser by itself does not provide an effective treatment for refractory melasma or postinflammatory hyperpigmentation.

Nigral degeneration in acquired immune deficiency syndrome (AIDS)

Using stereological techniques we have estimated the volume density of melanin and counted the number of pigmented and non-pigmented neuronal cell bodies in the pars compacta of the substantia nigra of 12 autopsied patients with acquired immune deficiency syndrome (AIDS) who did not have inflammation or necrosis of the midbrain or clinical parkinsonism. The total number of neuronal cell bodies was 25% lower in AIDS (P less than 0.01) than in 12 age-matched controls, although the volume density of neuronal melanin did not differ from that of controls because the percentage of pigmented cell bodies was higher (P less than 0.01) and the cell bodies were more fully packed with melanin in AIDS. Also, the expected increase with age of the volume density of neuronal melanin (P less than 0.02) and the percentage of pigmented neurons (P less than 0.01) occurred in the controls but not in AIDS patients. Importantly, our histopathological examination showed unequivocal nigral degeneration with neuronal loss, small neuronal cell bodies packed with melanin, reactive astrocytosis and extra-cellular melanin in the AIDS patients but not in controls. Our study shows that a subclinical nigral degeneration is common in AIDS and could possibly explain the heightened susceptibility of some patients to drug-induced parkinsonism.

Évolution simultanée d'une sclérose latérale amyotrophique, d'un syndrome parkinsonnien et d'une démence progressive: A propos de deux observations anatomo-cliniques Essai d'interprétation

Both of the 2 cases reported were characterized by the association of amyotrophic lateral sclerosis (A.L.S.) (which was the initial symptom in the first case), with an extra-pyramidal syndrome and progressive dementia (which was the first symptom in the second one). After respective illnesses of 2 and 3 years' duration, the patients died from labio-glosso-laryngeal paralysis. The pathological findings were those usually observed in A.L.S. and in Parkinsonism (neuronal loss and gliosis in the substantia nigra with extracellular melanin, but without Lewy bodies or neurofibrillary changes). In spite of clinical similarities, the absence of these latter pathological findings did not allow us to regard these cases as being examples of the A.L.S. - Parkinsonism-dementia complex seen on the island of Guam. The lesions in the cerebral cortex (areas of neuronal loss mainly in the second and third layers, associated with a slight and non-specific astrocytic gliosis) were not those of Pick's or Alzheimer's diseases, which are known sometimes to be associated with A.L.S. Our 2 cases are different from Jakob-Creutzfeldt disease clinically (no abnormal movements, no myoclonus, normal EEG and longer duration) and pathologically (there was slight spongiosis of the second cortical layer, very different from that seen in the Jakob-Creutzfeldt disease; slight astrocytic gliosis, without any rosettes or columns; no lesions in thalamus and putamen). However, clinical and pathological findings similar to those found in our cases may be found in amyotrophic forms of the Jacob-Creutzfeldt disease and their links with “spastic-pseudo-sclerosis” are doubtful. It seems impossible to look at these pathological associations as mere coincidences. However, A.L.S. and Parkinsonism are two systematic degenerative conditions, so their occasional association is not surprising in a genetic perspective.