EFEITOS DA INGESTÃO DE MICROPLÁSTICOS DE POLIETILENO EM FILHOTES DE Podocnemis expansa (TESTUDINES: PODOCNEMIDIDAE)

Abstract

Plastics are synthetically produced from polymers such as polyethylene, and their environmental degradation can produce fragments smaller than 5mm known as microplastics. Improperly discarded in aquatic environments, they pose a threat to the health of organisms like turtles. Amazonian turtle (Podocnemis expansa) populations are considered conservation-dependent, making it crucial to identify the impacts of emerging contaminants on this species. Given the harmful effects of microplastics, this study aimed to assess the effects of polyethylene microplastic (PE MP) exposure on the gastrointestinal tract and liver of P. expansa hatchlings. Forty-eight Amazonian turtle hatchlings were acclimated and distributed into six aquaria (n=8 per aquarium) corresponding to three experimental groups: I – control/no exposure to PE MP, II – exposure to PE MP once a week, and III – exposure to PE MP four times a week. PE MP was incorporated into commercial Nutripiscis® AL45 feed at a dose of 100 mg kg-1. The feed was provided daily at 5% of the hatchlings’ body weight. Control group individuals were fed with feed without added PE MP. After 30 days of exposure, animals were anesthetized with 2% xylazine and ketamine and euthanized (CEUA no. 23105.020525/2023-93). The liver was collected and weighed to determine the hepatosomatic index. Subsequently, the liver and gastrointestinal tract (stomach, small and large intestines) were conventionally processed for histology, and slides were stained with Hematoxylin and Eosin. Organs were semi-quantitatively evaluated using the Histopathological Alteration Index (HAI). To compare HAI among the three treatments, the non-parametric Kruskal-Wallis test and Dunn’s post-hoc test were used (p<0.05). In the groups exposed to PE MP (II and III), liver tissue showed damages such as cellular and nuclear hypertrophy, vacuolization, and cytoplasmic degeneration of hepatocytes, along with pyknotic nuclei and necrosis, with a significant increase in these alterations in group III (p=0.009). In the stomach, HAI was significantly higher in group III (p=0.001) compared to the control group. In the regions of the pyloric (stomach-small intestine) and ileocecal sphincters (small intestine-large intestine), increased foci of leukocyte infiltration indicated inflammation. In the small intestine, leukocyte infiltration foci were observed in the mucosa and submucosa, along with vessel dilation and edema in the submucosa. In the large intestine, leukocyte infiltration and mucous cell hyperplasia were observed in group III hatchlings. Although histopathological alterations along the gastrointestinal tract occurred across all treatments, they were more frequent and intense in hatchlings exposed to PE MP (groups II and III, p<0.05). This pattern would likely be observed in the small intestine of turtles with prolonged PE MP exposure, directly compromising nutrient absorption, potentially leading to weight loss, carapace growth retardation, and possibly death from malnutrition. These initial results further underscore the importance of assessing how increasing microplastic pollution affects freshwater biota.