These cytokines can promote progressive fibrosis and may diminish the capacity of macrophages to phagocytize and destroy infectious agents.
Carotenoid pigments, such as β-carotene, impart a yellow coloration to plasma, adipose tissue, and other lipid-laden cells. This discoloration is a dietary indicator and not a lesion.
Tetracycline binds to calcium phosphate in teeth and bones, resulting in permanent discoloration if administered during the time of mineralization.
Tetracycline therapy during their development.
Melanin is responsible for the color of the hair, skin, and iris, and also colors the leptomeninges in sheep and cattle with pigmented haircoats.
Localized deposits of melanin are called melanosis.
Melanocytes are derived from the neural crest and migrate to the site of pigment production during embryonic development.
Anthracosis is a form of pneumoconiosis caused by the inhalation of carbon particles, commonly seen in coal miners.
Carbon particles impart a fine gray-black stippling to the lung and cause dark-gray discoloration of tracheobronchial lymph nodes. They are phagocytized by macrophages and transported to bronchus-associated lymphoid tissue and tracheobronchial lymph nodes.
Histologically, carbon particles appear as fine black granular material and crystalline material in macrophages adjacent to intrapulmonary airways and vasculature.
Hepatocellular injury that decreases the uptake, conjugation, or secretion of bilirubin.
Numerous hemosiderin-laden alveolar macrophages.
Hematoidin is a bright-yellow crystalline pigment derived from hemosiderin, deposited in tissues at sites of hemorrhage.
Ferritin binds free iron and stores it in a nontoxic form available for use by the cell.
Reduced outflow of bile from the liver into the intestine due to an obstruction.
Nitrite oxidizes the iron in the heme group of hemoglobin to the Fe +3 (ferric) state, converting hemoglobin to methemoglobin, which has a low affinity for oxygen.
Icterus, or jaundice, is caused by elevated bilirubin concentration in the blood, leading to yellow staining of tissues.
A defective ATP-dependent transport system for various organic anions, including bilirubin diglucuronide.
Oxyhemoglobin, formed when oxygen binds to the heme group, gives oxygenated blood its red color. Deoxygenated hemoglobin explains the blue cast to venous blood.
Hemoglobin, bilirubin, and hemosiderin, respectively.
Hemosiderin is an intracellular iron storage complex, commonly found in macrophages, hepatocytes, and renal tubular epithelial cells.
Bilirubin is a breakdown product of erythrocytes, formed within macrophages after the removal of iron from hemoglobin.
The enzyme tyrosinase catalyzes the first step in melanin synthesis. A lack of tyrosinase results in albinism.
Carbon monoxide binds to hemoglobin with a much higher affinity than oxygen, forming carboxyhemoglobin, which colors the blood bright cherry red.
Cherry red
Heme oxygenase converts heme to biliverdin.
Lipofuscin accumulation in the canine myocardium has a linear correlation with the age of the dog.
Erythrocytes are lysed within vessels, releasing hemoglobin which imparts a transparent pink tinge to the plasma or serum.
The renal parenchyma turns a dark red to gunmetal blue.
Hemolysis or any process that increases the turnover of erythrocytes, delivering more unconjugated bilirubin to the liver than it can accommodate.
The presence of hemosiderin-laden macrophages can indicate chronic passive congestion.
Ceroid is a lipofuscin-like pigment that accumulates in disease states such as neuronal ceroid-lipofuscinosis, cachexia, vitamin E deficiency, or other oxidative stress.
Prehepatic, hepatic, and posthepatic.
Lipofuscin has an excitation wavelength between 320 and 480 nm and an emission wavelength between 460 and 630 nm.
Partial albinism in CHS is caused by a mutation of the LYST gene that codes for a lysosomal trafficking regulator protein.
Carboxyhemoglobin
The blackening is caused by hematin pigment excreted by migrating trematode larvae.
Cyanide blocks oxidative phosphorylation, preventing cells from using oxygen in hemoglobin, causing venous blood to be as red as arterial blood.
Methemoglobin turns the color of blood to a chocolate brown.
Porphyria is a heme synthesis disorder resulting in the deposition of porphyrin pigments in tissues, caused by genetic defects such as a deficiency of uroporphyrinogen III synthase.
In vitiligo, normally pigmented skin and hair become depigmented due to an immune-mediated attack on melanocytes or basilar keratinocytes.
The bluish discoloration is caused by hemoglobinuria, where hemoglobin is excreted via the kidney.
Acid hematin can be removed by soaking the dewaxed tissue section in a saturated alcoholic solution of picric acid.
Lipofuscin has a granular appearance ultrastructurally, while ceroid is more likely to form membranous stacks or whorls. Lectin histochemistry can also distinguish them by their sugar moieties.
Hematin, a brown-black, Fe +3-containing pigment.
Lipofuscin is a yellow-brown lipoprotein that accumulates as residual bodies in secondary lysosomes, especially in long-lived postmitotic cells such as neurons and cardiac myocytes.
Acid hematin is a dark brown to nearly black pigment that forms in tissues fixed in unbuffered, acidic formalin (pH < 6).
Hematogenous pigments are derived from erythrocytes and include hemoglobin, hematins, hemosiderin, hematoidin, bilirubin, biliverdin, and porphyrins.
Hyperpigmentation implies excessive melanin and is often associated with endocrine skin disease, especially hyperadrenocorticism.
Nitrite poisoning can be caused by consumption of nitrate-accumulating plants or contaminated water, leading to reduced oxygen transport in the blood.
