[1] The origin of these dense granules is still unknown, however, it is thought that may come from the mechanism involving the endocytotic pathway.

When the parasite invades it releases its dense granules which help to create the parasitophorous vacuole.

Dense granules, along with other secretory vesicles such as a microneme and rhoptry secrete proteins involved in the gliding motility, invasion, and parasitophorous vacuole formation of Toxoplasma gondii.

Dense granules specifically secrete their contents several minutes after parasite invasion and localization into the parasitophorous vacuole.

Proteins released from these specialized organelles are critical to adapting to the intracellular environment of the invaded host cell and contribute to parasitophorous vacuolar structure and maintenance.

[8] Additionally, dense granule formation follows a clathrin dependent matter at the trans-golgi network.

After clathrin is recruited, the mature dense granules bud off the golgi apparatus and are shuttled to plasma membrane release sites in order to secrete their contents.

[10] Many GRA proteins contain a single transmembrane domain, meaning that the proteins are translocated across the endoplasmic reticulum lumen, exported to and shuttled through the golgi apparatus, and eventually secreted from the parasite into the vacuolar space or parasitophorous vacuolar membrane.

Despite GRA proteins accumulating rapidly as a “burst” after a few minutes into invasion to help facilitate the newly formed parasitophorous vacuole similarly to a regulated secretory event, secretion of GRA proteins is a constitutive process independent of calcium occurring throughout the parasite's life cycle both intracellularly and extracellularly.

[12] According to the stage of infection, the number of dense granules present in a parasite may vary from approximately 15 in tachyzoites and sporozoites, 8–10 in bradyzoites and 3–6 in merozoites.

[7][10] In order to scavenge and sequester host cells’ nutrients and lipids, the intravacuolar network (IVN) must first be formed by T. gondii.

This network of membranous tubules is involved in acquiring nutrients, modulating immune response, and facilitating cyst development.

[3] The serotonin that is then released by the dense granule, recruits other platelets and helps play a major role in stopping the loss of blood at the injury.

[17] The patients with this disease show signs of abnormal dense granules and melanosomes which can cause prolonged bleeding and albinism.

Chediak-Higashi syndrome is an autosomal recessive disorder where patients platelets have a deficient amount of dense granules.

Since dense granules have surface membrane proteins, the activation of CD63 and LAMP-2 can be observed with flow cytometry.