According to the World Health Organization (WHO), based on the limited amount of data available, there is a very low probability that microplastic particles entering the body with drinking water pose a risk to human health. At the same time, it is worrying that nanoplastic particles are also present in our drinking water, and their absorption seems plausible due to their size. Therefore, attention is drawn to the importance of taking action against microplastic pollution and researching the occurrence, potential impact on human health, and elimination of micro(nano)plastics [114]. Based on the limited animal study data, it seems that microplastic particles that enter the living organism usually pass through the digestive tract and are excreted with the feces. However, some particles accumulate and get stuck in the digestive tract, causing blockages and preventing the organism from further absorbing food. The accumulation of microplastic particles as foreign bodies in the intestinal tract activates the body’s immune system and induces local inflammation. The resulting chronic inflammation impairs the function of the intestinal system. The toxic effect of nanoplastics is more pronounced than that of microplastics due to their smaller size, which facilitates easier absorption from the intestine into the bloodstream, passage through biological membranes, and accumulation in organs [7]. When microplastics accumulate in peripheral organs, they trigger a local immune response and inflammation, causing damage to the affected organ and impairing its function. In rodents, the absorbed microplastics accumulated in the liver and kidneys, leading to oxidative stress, inflammation, and neurotoxicity [98]. Oxidative stress can result from oxidizing substances bound to the relatively large surface area of microplastics, such as heavy metals, or from reactive oxygen radicals (ROS) released during inflammatory processes. Cellular uptake of PS microparticles was observed in rat macrophages, red blood cells, and alveolar epithelial cell cultures. Inside the cell, the microplastic was not bound to the membrane but interacted with cell organelles. In macrophages, microplastic exposure resulted in cell death due to endoplasmic reticulum stress and release of ROS [16], [108]. The toxic effect of aged microplastic particles is enhanced because the higher the degree of microplastic degradation, the more reactive oxygen radicals the polymer contains, thus increasing the health hazard [74]. As a result of microplastic exposure, the upregulation of the CYP 450 enzymes responsible for the elimination of toxic substances, namely the cyp1a gene, as well as certain DNA repair genes (xrcc2, lmx1ba, etv2, e2f8) were observed. In fish, microplastics caused immunotoxicity and activated genes related to the complement system and innate immune system [102]. In animal studies, abnormal embryonic development, malformations, decreased appetite, slowed growth, weight loss, altered reproduction, damaged intestinal microvilli, decreased lysosomal membrane stability, DNA damage, decreased oocyte number and size, decreased sperm number and motility, increased glycolysis, tissue necrosis, arrithmia, altered brain water content, and death have also been described as a result of microplastic exposure [44], [110]. In these animal models, altered gene expression of heat shock proteins responsible for the stress response and increased mortality of hemocytes and granulocytes have been demonstrated following microplastic administration [110]. Impaired immune functions and pulmonary hypertension have also been observed in animals exposed to microplastics [108]. Energy metabolism may also be disrupted under the influence of microplastics. An increase in the activity of the enzyme lactate dehydrogenase, modulation of the RNA of PPAR receptors involved in lipid metabolism, as well as a decrease in ATP content in the liver, have also been observed in mice exposed to microplastics [16], [97]. In animal models, PS nanoparticles activated oxidative stress-induced MAPK/Nrf2 signaling, increased the activity of some antioxidant enzymes (SOD, CAT, GPX, GST) and decreased the level of reduced glutathione, stimulated the expression of cas8 gene, which plays a role in the control of apoptosis, [97], [101], [102], [110]. Nanoplastics induce changes in the gene expression of estrogen receptors, and alterations in the activity of the lipid peroxidase, CYP 450 1A1, citrate synthase and cytochrome c oxidase enzymes. Moreover, they increase the amounts of IgM type antibodies, along with IL -1a and IL -1b inflammatory cytokines in the intestine [110]. Aminated polystyrene nanoparticles altered the feeding behavior, caused apoptosis of red blood cells, provoked oxidative stress in mollusks, and induced embryotoxicity in sea urchin embryos [104]. Neurotoxic effects of nanoparticles have been shown in zebrafish, namely decreased acetylcholinesterase enzyme activity and inhibition of dopamine, melatonin, serotonin, vasopressin, kisspeptin, and oxytocin [102].