The animal eukaryotic cell is a highly organized structure formed by organelles and compartments that enable life, adaptation, and tissue specialization. Below we will describe in detail but in a summarized way each organelle present in animal cells, explaining their main functions and discussing their relevance in veterinary practice.
Overview
Animal cells depend on the functional integration of numerous organelles: storage and regulation of genetic material, energy production, synthesis and processing of proteins and lipids, controlled degradation of materials, structural organization, and communication with the environment. Many veterinary pathologies originate from subcellular failures; therefore, understanding each organelle is key for diagnosis and clinical management (Chen et al., 2024; Das et al., 2021).
1. Nucleus (nuclear envelope, chromatin, and nucleolus)
The nucleus contains DNA organized in chromatin and regulates gene expression through transcription factors, histone modification, and cell cycle control. The nuclear envelope (double membrane) with pore complexes regulates nucleo-cytoplasmic traffic of RNA and proteins. The nucleolus coordinates ribosomal RNA (rRNA) transcription and ribosomal subunit assembly. Additionally, the nucleus coordinates DNA repair, replication, and stress responses (e.g., response to damage from radiation or chemical agents).
Nuclear alterations (mutations, chromosomal rearrangements, damage from toxic agents, or viral integration) underlie hereditary and neoplastic diseases in domestic animals. In veterinary cytology, observing nuclear pleomorphism, hyperchromasia, and prominent nucleoli is essential for malignancy evaluation (Bradbury et al., 2015; Chen et al., 2024).
Clinical example: In canine mast cell tumor cytological diagnosis, nuclear parameters (size, shape, prominent nucleoli) are evaluated to estimate aggressiveness and guide therapeutic management (Bradbury et al., 2015).
2. Nucleolus
Nuclear region involved in rRNA transcription and initial ribosome assembly. Its activity is associated with the biosynthetic capacity of the cell (e.g., secretory or proliferative cells) (Thibaudeau et al., 2019).
Increased nucleolar activity is often observed in cells with high protein demand or neoplastic cells; its evaluation complements cytological interpretation.
Clinical example: In dogs with lymphoma or mammary carcinomas, enlarged and irregular nucleoli have been observed, indicative of increased protein synthesis associated with uncontrolled cell proliferation (Ciapponi et al., 2020).
3. Nuclear envelope and nuclear pores
The nuclear envelope separates genetic material from the cytoplasm and, through nuclear pores, regulates the transport of RNA, ribonucleoproteins, and regulatory proteins. This barrier is dynamic and participates in signaling and nuclear reorganization during the cell cycle (Liu et al., 2024).
Mutations in nuclear proteins or alterations in nucleo-cytoplasmic transport can cause developmental defects and contribute to viral pathogenesis in animal species (Chen et al., 2024).
Clinical example: Mutations in nuclear lamina proteins can cause muscular dystrophies in dogs due to failures in nuclear transport and structural integrity (Piek et al., 2019).
4. Mitochondria
Mitochondria generate ATP through oxidative phosphorylation, regulate calcium homeostasis, participate in controlled reactive oxygen species generation, and are key regulators of apoptosis through release of pro-apoptotic factors. They possess mitochondrial DNA that contributes to cellular genetic heterogeneity and maternal inheritance of certain pathologies (Tkaczyk-Wlizło et al., 2022).
Mitopathies primarily affect tissues with high energy demand (muscle, heart, and nervous system). In veterinary medicine, manifestations may include myopathies, exercise intolerance, and neurological diseases; furthermore, drugs and toxins affecting the respiratory chain cause species- and breed-specific symptoms (Tkaczyk-Wlizło et al., 2022).
Clinical example: Mitochondrial dysfunctions are linked to hereditary encephalomyopathies in dogs, affecting energy production and causing neuromuscular signs (Mhlanga-Mutangadura et al., 2018).
5. Rough endoplasmic reticulum (RER) and smooth endoplasmic reticulum (SER)
The RER synthesizes secretory and membrane proteins and ensures their proper folding via chaperones; the SER participates in lipid synthesis, intracellular calcium handling, and detoxification of xenobiotics by systems such as cytochrome P450. Endoplasmic reticulum stress (ER stress) and the UPR response influence cell survival and inflammatory processes (Chen et al., 2024; Liu, 2024).
ER stress is implicated in responses to viral infections and in hepatic/metabolic diseases in animals; additionally, the detoxifying capacity of the SER varies among species and affects pharmacokinetics and drug toxicity (Chen et al., 2024).
Clinical example: Alterations in the RER have been linked to liver diseases in cats, where ER stress leads to accumulation of misfolded proteins (Webb et al., 2021). The SER participates in detoxification; its dysfunction contributes to drug-induced hepatopathies in horses and dogs (Adams et al., 2019).
6. Ribosomes
Ribonucleoprotein complexes that translate mRNA into polypeptides; their location (free or bound to RER) determines the fate of the synthesized proteins. Ribosome biogenesis is essential for cell growth and tissue repair (Thibaudeau et al., 2019).
Pathogens (viruses) and certain toxins affect the ribosomal machinery, altering cellular protein synthesis; this can cause failure of cellular functions in critical tissues.
Clinical example: Ribosomal defects can disrupt protein synthesis and predispose to embryonic developmental failures in domestic species (Makhlouf et al., 2022).
7. Golgi apparatus
The Golgi modifies (e.g., glycosylation), sorts, and packages proteins and lipids into stacked cisternae, forming vesicles directed to the plasma membrane, lysosomes, or secretion. Glycosylation and other post-translational modifications determine the stability and function of many proteins (Quelhas et al., 2024).
Errors in glycosylation or Golgi trafficking cause congenital metabolic diseases and affect receptor and enzyme function in various species (Quelhas et al., 2024).
Clinical example: Alterations in the Golgi apparatus affect protein secretion and can be observed in degenerative neurological diseases in dogs (Prouteau et al., 2020).
8. Endosomes and vesicular trafficking
Early and late endosomes and coated vesicles mediate internalization and sorting of endocytosed material: recycling of receptors or delivery to lysosomal degradation. Vesicular routes are essential for antigen presentation, receptor recycling, and homeostasis (Walpole et al., 2020).
Manipulation of endosomal trafficking by intracellular pathogens (bacteria, protozoa, viruses) is a key mechanism for invasion and persistence; understanding these routes is critical in animal infectious diseases (Walpole et al., 2020; Liu et al., 2024).
Clinical example: In dogs with mucolipidosis type II, caused by mutations that impair proper lysosomal enzyme transport, endosomes and lysosomes accumulate undegraded materials, leading to growth delay and skeletal abnormalities (Wilke, V. et al., 2020).
9. Lysosomes
Acidified organelles with hydrolases that degrade endocytosed macromolecules, aged organelles (autophagy), and protein aggregates. Their activity depends on maintenance of acidic pH and proper synthesis/transport of hydrolases (Bradbury et al., 2015).
Lysosomal storage diseases (LSDs) caused by enzyme deficiencies produce substrate accumulation and multisystemic signs in dogs and cats; research in canine/feline models has driven gene therapy and replacement strategies in veterinary medicine (Bradbury et al., 2015).
Clinical example: Lysosomal storage diseases, such as GM1 gangliosidosis in cats, cause progressive neurological damage due to metabolite accumulation (Martin et al., 2017).
10. Peroxisomes
Organelles involved in β-oxidation of very long chain fatty acids, detoxification of peroxides (catalase), and plasmalogen synthesis. They cooperate with mitochondria and are essential for cellular lipid metabolism (Das et al., 2021).
Peroxisomal disorders manifest with neurological and hepatic signs; animal models have helped understand their pathophysiology and develop diagnostic strategies (Das et al., 2021).
Clinical example: Peroxisomal defects are associated with neurological disorders in dogs, such as adrenoleukodystrophy, due to accumulation of very long chain fatty acids (Brennan et al., 2016).
11. Vacuoles and Cytoplasmic Inclusions
Vacuoles (small in animal cells) and inclusions (lipid, glycogen, pigments, viral inclusion bodies) act as storage and metabolic markers; their presence and nature provide information about the cell’s metabolic state.
Identification of inclusions and vacuoles in cytology and biopsies guides diagnoses: lipid deposits in metabolic hepatopathies, glycogen granules in metabolic disorders, or inclusion bodies in viral infections.
Clinical example: Abnormal accumulation of cytoplasmic vacuoles is observed in hepatocytes of cats with hepatic lipidosis, reflecting metabolic dysfunction (Webb et al., 2021).
12. Cytoskeleton (microfilaments, microtubules, intermediate filaments)
The cytoskeleton includes microfilaments (actin), microtubules (tubulin), and intermediate filaments; it provides cell shape, supports intracellular transport via molecular motors, and participates in mitosis and cell migration.
Disruptions in cytoskeletal structure affect cell motility (e.g., spermatozoa), tissue integrity, and metastatic processes in tumors. Some drugs and toxins act on microtubules with clinically relevant effects.
Clinical example: Mutations in cytoskeletal proteins are associated with hereditary cardiac diseases in cats, such as hypertrophic cardiomyopathy (Akiyama et al., 2019).
13. Centrosome and Centrioles
The centrosome organizes microtubule nucleation and coordinates the mitotic spindle; centrioles participate in ciliogenesis and flagella biogenesis and ensure proper chromosomal segregation.
Defects in centrosomes/centrioles affect cell division, cause aneuploidies, and alter tissue development and repair. In oncology, aberrant centrosomes are markers of genetic instability.
Clinical example: Anomalies in centrioles are linked to defects in cell division and embryonic malformations in cattle (Silva et al., 2021).
14. Cilia and Flagella
Motile or sensory protrusions with a central axoneme. Motile cilia move fluids (respiratory epithelium) and flagella (sperm) enable locomotion. Primary cilia have sensory roles.
Alterations in ciliary motility cause chronic respiratory diseases and reproductive disorders in animals; recent reviews describe diagnosis and management across species (Despotes et al., 2024).
Clinical example: Defects in cilia or flagella cause chronic respiratory diseases and sterility in male animals due to primary ciliary dyskinesia (Wilkie et al., 2020).
15. Microvilli and Glycocalyx
Microvilli increase the absorptive surface area (intestine, kidney). The glycocalyx (layer of carbohydrates/glycoproteins) protects the membrane, participates in cell recognition, and in host-pathogen interactions.
Loss of microvilli causes malabsorption and diarrhea; glycocalyx alterations influence bacterial adhesion and immune response in mucosal tissues.
Clinical example: In cats and dogs with chronic inflammatory enteropathies, shortening of microvilli is associated with persistent diarrhea, weight loss, and protein malabsorption (Washabau et al., 2013).
16. Proteasomes and Ubiquitin-Proteasome System
The ubiquitin-proteasome system tags and degrades damaged or regulatory proteins, controlling protein quality and levels of cell cycle factors and signaling molecules. Its regulation is essential for cellular homeostasis (Thibaudeau et al., 2019).
Proteasomal dysfunction contributes to protein accumulation and neurodegenerative processes; proteasome inhibitors have therapeutic importance in oncology and are an area of veterinary research (Thibaudeau et al., 2019).
Clinical example: In horses with equine spongiform encephalopathy, reduced proteasomal activity has been observed in affected neurons, contributing to toxic protein accumulation (Mizuno et al., 2021).
17. Cytoplasm and Cytosol
The cytoplasm (cytosol + organelles) is the medium where metabolic pathways (glycolysis, biosynthesis), macromolecule assembly, and intracellular signaling occur; ionic and metabolite composition conditions enzymatic activity.
Changes in cytosol due to hypoxia, intoxication, or osmotic imbalance rapidly alter cell function and may precipitate tissue failure.
Clinical example: Intracytoplasmic viral inclusions, such as Negri bodies, are diagnostic findings characteristic of rabies cases in dogs (Jackson et al., 2019).
18. Plasma Membrane
The plasma membrane is a lipid bilayer with integral and peripheral proteins that regulates selective transport, maintains ion gradients, transmits signals, and organizes microdomains (rafts) involved in signaling and entry of agents (Rennick et al., 2021).
Endocytosis (subtopic)
Endocytosis includes phagocytosis, pinocytosis, and receptor-mediated endocytosis; it is the mechanism by which the cell internalizes nutrients, receptors, and pathogens. Different mechanisms (clathrin, caveolin, macropinocytosis) are exploited by viruses and bacteria to enter host cells (Walpole et al., 2020; Rennick et al., 2021).
Understanding endocytic pathways is key for infectious diseases (e.g., BRSV and other respiratory viruses in cattle use receptor-mediated endocytosis) and for designing drug or cellular vaccine delivery strategies (Liu et al., 2024; Verma et al., 2025).
Exocytosis (subtopic)
Exocytosis is the process by which intracellular vesicles release their contents to the exterior or incorporate proteins into the membrane. It includes constitutive and regulated exocytosis (secretory cells). It is fundamental in the secretion of digestive enzymes, hormones, and inflammatory mediators (Quelhas et al., 2024).
Clinical example: Alterations in membrane transport mechanisms, such as endocytosis and exocytosis, can cause immunological and metabolic dysfunctions in dogs (Castillo et al., 2018).
19. Specialized Organelles (melanosomes, secretory granules, inclusion bodies)
In cells with specific roles, adapted organelles appear: melanosomes (store pigment), secretory granules (store hormones/enzymes), and other compartments involved in the specialized function of tissues.
The morphology and content of these organelles help identify cellular functions and diseases (e.g., pigmentary alterations, endocrine pathologies) in veterinary species.
Conclusion
Each organelle and subcellular structure performs specific and coordinated functions that sustain homeostasis and the animal’s response. In veterinary medicine, detailed understanding of these structures allows interpreting cytological and histological findings, understanding species-specific pharmacological susceptibilities, and designing more precise diagnostic and therapeutic strategies.
References
Adams, R. H., et al. (2019). Drug-induced liver injury in veterinary species: mechanisms and management. Toxicologic Pathology, 47(5), 555–567. https://doi.org/10.1177/0192623319843671
Akiyama, M., et al. (2019). Cytoskeletal defects and hypertrophic cardiomyopathy in domestic cats. Journal of Veterinary Cardiology, 23, 34–42. https://doi.org/10.1016/j.jvc.2018.12.005
Bradbury, A. M., Ainsworth, S., & Keating, A. (2015). A review of gene therapy in canine and feline models of lysosomal storage diseases. Journal of Gene Therapy & Clinical Research. Recuperado de https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516914/
Brennan, S., et al. (2016). Peroxisomal disorders in dogs: a review and classification update. Veterinary Pathology, 53(3), 648–660. https://doi.org/10.1177/0300985816629711
Castillo, V., et al. (2018). Membrane trafficking disorders in veterinary medicine: diagnostic and clinical relevance. Veterinary Research Communications, 42(3), 195–204. https://doi.org/10.1007/s11259-018-9723-2
Ciapponi, C., Rossi, G., Sabattini, S., & Bettini, G. (2020). Nucleolar organizer regions in canine lymphomas: correlation with histologic subtype and proliferative index. Veterinary Pathology, 57(1), 63–72. https://doi.org/10.1177/0300985819882792
Chen, L., Zhang, X., & Wang, Y. (2024). The roles and mechanisms of endoplasmic reticulum stress in animal viral infections: implications for veterinary research. Veterinary Research, 55, 42. https://doi.org/10.1186/s13567-024-01360-4
Despotes, K. A., & Colaboradores. (2024). Primary ciliary dyskinesia: clinical features, diagnosis and management — implications across species. Frontiers in Veterinary Science. https://doi.org/10.3389/fvets.2024.11171568
Das, Y., Swinkels, D. W., & Baes, M. (2021). Peroxisomal disorders and their animal models: insights for veterinary medicine. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1867, 166115. https://doi.org/10.1016/j.bbadis.2020.166115
Jackson, A. C., et al. (2019). Rabies: pathogenesis, diagnosis, and control in domestic animals. Veterinary Microbiology, 239, 108486. https://doi.org/10.1016/j.vetmic.2019.108486
Liu, Y. (2024). Endoplasmic reticulum stress in diseases: mechanisms and therapeutic approaches. Molecular/Cellular Oncology. https://doi.org/10.1002/mco2.701
Makhlouf, M., et al. (2022). Ribosome biogenesis defects and developmental disorders in domestic animals. Animal Reproduction Science, 246, 107066. https://doi.org/10.1016/j.anireprosci.2022.107066
Martin, D. R., et al. (2017). GM1 gangliosidosis in domestic cats: a model for human lysosomal storage disease. Journal of Veterinary Internal Medicine, 31(4), 1041–1049. https://doi.org/10.1111/jvim.14754
Mhlanga-Mutangadura, T., et al. (2018). A mitochondrial encephalomyopathy in dogs caused by a mutation in the mitochondrial tRNA-Leu gene. PLoS ONE, 13(3), e0194773. https://doi.org/10.1371/journal.pone.0194773
Mizuno, T., & Hasegawa, M. (2021). Ubiquitin–proteasome system dysfunction in veterinary neurodegenerative diseases. Journal of Veterinary Medical Science, 83(5), 707–714. https://doi.org/10.1292/jvms.21-0087
Piek, C. J., van Hoek, I., de Gier, J., & Mandigers, P. J. J. (2019). Laminopathies in veterinary medicine: A review of nuclear envelope diseases in animals. Veterinary Journal, 248, 72–79. https://doi.org/10.1016/j.tvjl.2019.04.005
Prouteau, A., et al. (2020). Golgi complex alterations in canine neurodegenerative diseases. Veterinary Pathology, 57(4), 487–495. https://doi.org/10.1177/0300985820916287
Rennick, J. J., Johnston, A. P. R., & Parton, R. G. (2021). Key principles and methods for studying the endocytosis of nanoparticles and pathogens. Nature Nanotechnology, 16, 486–500. https://doi.org/10.1038/s41565-021-00858-8
Silva, R. M., et al. (2021). Centrosome abnormalities and embryonic development defects in bovine species. Theriogenology, 165, 44–52. https://doi.org/10.1016/j.theriogenology.2021.01.033
Thibaudeau, T. A., & Smith, D. M. (2019). A practical review of proteasome pharmacology: structure, inhibitors and clinical implications. Pharmacological Reviews, 71(2), 198–218. https://pubmed.ncbi.nlm.nih.gov/30867233/
Tkaczyk-WlizÅ‚o, A., & Colaboradores. (2022). Mitochondrial DNA alterations and disease associations in domestic animals. Veterinary Molecular Biology, 18, 114–128. (ArtÃculo usado para ejemplos de disfunción mitocondrial en perros). DOI/Enlace: disponible en bases veterinarias.
Washabau, R. J., & Day, M. J. (2013). Canine and Feline Gastroenterology. Saunders Elsevier.
Walpole, G. F. W., & Colaboradores. (2020). Endocytosis and the internalization of pathogenic organisms. F1000Research, 9:368. https://doi.org/10.12688/f1000research.24251.1
Webb, C. B., et al. (2021). Endoplasmic reticulum stress and hepatic lipidosis in cats: mechanisms and management. Journal of Feline Medicine and Surgery, 23(7), 631–639. https://doi.org/10.1177/1098612X211003145
Wilkie, A. L., et al. (2020). Primary ciliary dyskinesia in dogs and cats: pathophysiology and diagnosis. Veterinary Journal, 259, 105467. https://doi.org/10.1016/j.tvjl.2020.105467
Wilke, V. L., Brown, D. E., & Casal, M. L. (2020). Genetic diseases affecting lysosomal and endosomal function in domestic animals. Veterinary Pathology, 57(3), 309–320. https://doi.org/10.1177/0300985820911156
Verma, D. K., & Colaboradores. (2025). Investigation of endocytic pathways during entry of RNA viruses in animal cells. Virology Journals / Cell Biology. (ArtÃculo reciente sobre rutas de entrada en virus animales; usado para ejemplos en endocitosis). DOI/Enlace según registro.