The effects of chronic lead exposure on the liver of female Japanese quail (Coturnix japonica): Histopathological damages, oxidative stress and AMP-activated protein kinase based lipid metabolism disorder.

Lead (Pb) is one of the most toxic metals to human and wildlife. It also had multiple negative influences on birds with physical, neurological and hematological clinical signs. However, the impacts of lead on bird liver lipid metabolism are still unclear. In this study, female Japanese quails were used to examine the effects of chronic lead exposure on liver histology, oxidative stress and AMPK (AMP-activated protein kinase) based lipid metabolism. Quails were randomly divided into 5 groups and each group was respectively fed with 0, 50, 250, 500 and 1000 ppm lead solution for 49 days. The result showed that exposure to 250, 500 and 1000 ppm Pb induced severe histopathological damages characterized by liver lipid vacuoles and accumulation, hepatic cytoplasmic hyalinization and vacuolization, hepatocytes necrosis, hepatic sinusoid congestion, and it also caused ultrastructural alterations featured by swelling and vacuolar mitochondria, the depolymerization of polyribosome, and lipid droplets accumulation. Moreover, significant decrease of activities of GPx (glutathione peroxidase), SOD (superoxide dismutase), CAT (catalase) and level of T-AOC (total antioxidant capacity) while significant increase of MDA (malondialdehyde) content were found in livers of all Pb groups. In addition, the expressions of genes related to fatty synthesis were significantly upregulated in livers of all Pb groups while the expressions of genes related to fatty ß-oxidation were significantly downregulated in livers of 250 ppm Pb group. The present study indicated lead exposure does cause bird health damages through inducing liver microstructural and ultrastructural injury, oxidative damages and lipid metabolism disorder.

The effects of chronic cadmium exposure on the gut of Bufo gargarizans larvae at metamorphic climax: Histopathological impairments, microbiota changes and intestinal remodeling disruption.

Cadmium (Cd) is carcinogenic to human and it also has adverse effects on aquatic life such as amphibian larvae. However, its influences on amphibian gut morphology and development as well as intestinal microbiota are still hardly understood. In this study, we examined the effects of chronic cadmium exposure on the gut of tadpoles at Gosner stage 42 of metamorphic climax by using Bufo gargarizans as a model species. Tadpoles were exposed to cadmium concentrations at 0, 5, 100 and 200 µg L-1 from Gosner stage 26-42. The results showed that high cadmium (100 and 200 µg L-1) exposure caused significant decrease of body length and weight but significant increase of intestinal length and weight. Moreover, severe histopathological damages were induced by high Cd exposure. In addition, microbial communities in the gut of tadpoles in high cadmium exposure groups were remarkably different from those in control group. Unexpectedly, species diversity and richness were higher in the intestinal microbiota of 200 µg L-1 cadmium exposure group. Furthermore, the abundance of prevalent phyla, families and genera of intestinal microbiota were changed by cadmium exposure. Meanwhile, cadmium exposure perturbed gut renewal functions and the relative mRNA expression of genes involved in canonical and non-canonical Wnt signaling pathway was seriously affected by high cadmium exposure. We concluded that cadmium could be harmful to tadpole health by inducing intestinal histopathological damages, gut remodeling inhibition and intestinal microbiota alterations.

Chronic lead exposure induces histopathological damage, microbiota dysbiosis and immune disorder in the cecum of female Japanese quails (Coturnix japonica).

Lead (Pb) is one of the most hazardous metals to human and wildlife and it also has multiple negative impacts on birds. However, its influences on bird gut morphology and intestinal microbiota were still unclear. We used female Japanese quails (Coturnix japonica) to examine the effects of chronic lead exposure (0, 50 ppm and 1000 ppm) on cecal histology, microbial communities and immune function. The results showed 50 ppm lead exposure caused subtle damages of cecum cell structure. However, 1000 ppm lead exposure caused severe cecum histopathological changes characterized by mucosa abscission, Lieberkühn glands destruction and lymphocyte proliferation. Moreover, both lead concentrations induced ultrastructural damages featured by nucleus pyknosis, mitochondrial vacuolation and microvilli contraction. Meanwhile, microbial community structure, species diversity, taxonomic compositions and taxa abundance in the cecum were affected by lead exposure. Furthermore, the mRNA relative expression of immunity-related genes such as interleukin 2 (IL-2) and gamma interferon (IFN-γ) was significantly downregulated while that of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and natural killer kappa B (NF-κB) was significantly upregulated in the cecum of 50 and 1000 ppm lead exposure groups. We concluded that lead exposure may cause gut health impairment of female Japanese quails by inducing cecal histopathological changes, microbiota dysbiosis and cecal immune disorder.

Chronic effects of mercury on Bufo gargarizans larvae: Thyroid disruption, liver damage, oxidative stress and lipid metabolism disorder.

Mercury is severely detrimental to organisms and is ubiquitous in both terrestrial and aquatic ecosystems. In the present study, we examined the effects of chronic mercury (Hg) exposure on metamorphosis, body size, thyroid microstructures, liver microstructural and ultrastructural features, and transcript levels of genes associated with lipid metabolism, oxidative stress and thyroid hormones signaling pathways of Chinese toad (Bufo gargarizans) tadpoles. Tadpoles were exposed to mercury concentrations at 0, 6, 12, 18, 24 and 30 µg/L from Gosner stage 26-42 of metamorphic climax. The present results showed that high dose mercury (24 and 30 µg/L) decelerated metamorphosis rate and inhibited body size of B. gargarizans larvae. Histological examinations have clearly exhibited that high mercury concentrations caused thyroid gland and liver damages. Moreover, degeneration and disintegration of hepatocytes, mitochondrial vacuolation, and endoplasmic reticulum breakdown were visible in the ultrastructure of liver after high dose mercury treatment. Furthermore, the larvae exposed to high dose mercury demonstrated a significant decrease in type II iodothyronine deiodinase (Dio2) and thyroid hormone receptor α and ß (TRα and TRß) mRNA levels. Transcript level of superoxide dismutase (SOD) and heat shock protein (HSP) were significantly up regulated in larvae exposed to high dose mercury, while transcript level of phospholipid hydroperoxide glutathione peroxidase (PHGPx) was significantly down regulated. Moreover, exposure to high dose mercury significantly down regulated mRNA expression of carnitine palmitoyltransferase (CPT), sterol carrier protein (SCP), acyl-CoA oxidase (ACOX) and peroxisome proliferator-activated receptor α (PPAPα), but significantly up regulated mRNA expression of fatty acid elongase (FAE), fatty acid synthetase (FAS) and Acetyl CoA Carboxylase (ACC). Therefore, we conclude that high dose mercury induced thyroid function disruption, liver oxidative stress and lipid metabolism disorder by damaging thyroid and liver cell structures and altering the expression levels of relevant genes.