The effects of chronic cadmium exposure on Bufo gargarizans larvae: Histopathological impairment, gene expression alteration and fatty acid metabolism disorder in the liver.

Cadmium (Cd) a highly toxic metal to human and wildlife health and it is hazardous to both terrestrial and aquatic life. In this study, we used RNA sequencing analysis to examine the effects of chronic cadmium exposure on liver lipid metabolism of Bufo gargarizans larvae. Tadpoles were exposed to cadmium concentrations at 0, 5, 10, 50, 100 and 200 µg L-1 from Gosner stage 26-42 of metamorphic climax. The results showed high dose cadmium (50, 100 and 200 µg L-1) caused obvious histological changes characterized by hepatocytes deformation, nuclear pyknosis, increasing melanomacrophage centers (MMCs) and aggregated lipid droplets. Moreover, transcriptome analysis showed that liver function was seriously affected by cadmium exposure. Furthermore, high dose cadmium significantly upregulated the mRNA expression of elongation of very-long-chain fatty acids 1 (ELOVL1), Mitochondrial trans-2-enoyl-CoA reductase (MECR), Trans-2, 3-enoyl-CoA reductase (TER) and Hydroxysteroid (17ß) dehydrogenase type 12 (HSD17B12) which are related with fatty acid synthesis. Meanwhile, mRNA levels of genes related with fat acid oxidation such as acetyl-CoA acyltransferase 2 (ACAA2) and enoyl-coenzyme A (CoA) hydratase short chain 1 (ECHS1) were significantly upregulated while the expression of Acyl-coA thioesterase 1 (ACOT1), 3-hydroxyacyl-CoA dehydrogenase (HADH), Palmitoyl-protein thioesterase 1(PPT1) and Acetyl-CoA acyltransferase 1(ACAA1) was significantly downregulated by high dose cadmium exposure. Furthermore, the mRNA level of ATP-binding cassette subfamily B member 11 (ABCB11) related with bile secretion was significantly decreased exposed to high dose cadmium. Our results suggested cadmium can cause liver dysfunction by inducing histopathological damages, genetic expression alterations and fatty acid metabolism disorder.

Exposure to cadmium induced gut histopathological damages and microbiota alterations of Chinese toad (Bufo gargarizans) larvae.

Cadmium (Cd) is highly hazardous to both terrestrial and aquatic life and it also has multiple negative impacts on amphibian tadpoles and frogs. However, its effects on gut health of amphibian tadpoles are still poorly understood. We used Chinese toad (Bufo gargarizans) tadpoles to examine the effects of chronic cadmium exposure on gut histology and intestinal microbiota by using regular histology analysis and high-throughput sequencing techniques. Tadpoles were exposed to cadmium concentrations at 0, 5, 100 and 200 µg L-1 from Gosner stage 26 to 38. Our results showed 100 and 200 µg L-1 cadmium exposure caused severe gut histopathological alterations while 5 µg L-1 cadmium exposure induced subtle intestine damage. Moreover, species diversity, taxonomic composition and community structure of gut microbiota were influenced by cadmium exposure. Species diversity and richness decreased gradually with the increase of cadmium concentration. Microbial communities of tadpoles in 100 and 200 µg L-1 cadmium exposure groups were remarkably different from those in control group. Furthermore, the relative abundances of prevalent phyla such as Proteobacteria, Bacteroidetes and Firmicutes and dominant genera such as Klebsiella and Aeromonas were also affected by cadmium exposure. We concluded that cadmium could be harmful to tadpole health by inducing intestinal damages and gut microbiota changes.

Effects of chronic cadmium exposure on metamorphosis, skeletal development, and thyroid endocrine disruption in Chinese toad Bufo gargarizans tadpoles.

The present study examined the effects of chronic cadmium (Cd) exposure on metamorphosis, body size, thyroid gland, and skeletal development of Chinese toad (Bufo gargarizans) tadpoles. Tadpoles were exposed to Cd concentrations at 0, 5, 10, 50, 100, and 500 µg/L from Gosner stages 26 to 46 of completion of metamorphosis. Our results showed that 100 and 500 µg/L of Cd concentrations increased mortality and decelerated metamorphosis rate. In addition, significant body size reduction at Gosner stage 42 was observed at 100 and 500 µg/L of Cd treatments (p < 0.01). Average body length and hind-limb length were significantly decreased in the 500 µg/L of Cd group (p < 0.05) but body mass was not significantly different at Gosner stage 46. Moreover, bone formation was delayed in high Cd concentration treatments (50, 100, and 500 µg/L) at both Gosner stage 42 and 46. Histopathological changes of the thyroid gland showed that follicular cell hyperplasia and malformation were induced by high Cd concentrations (50, 100, and 500 µg/L). Furthermore, real-time polymerase chain reaction analysis suggested that the larvae exposed to high-dose Cd exhibited a significant decrease in deiodinase (Dio2) and thyroid hormone receptor (TRß) mRNA levels at Gosner stage 42 and 46. Our investigation indicated that high-dose Cd caused metamorphic deceleration, body size reduction, and delayed skeletal development through disrupting the thyroid system in B. gargarizans larvae. Environ Toxicol Chem 2018;37:213-223. © 2017 SETAC.