To evaluate the renal toxicity of dietary aflatoxin B₁ (AFB₁) and ameliorating effects of added dietary sodium selenite in broiler, renal histopathological changes, ultrastructural changes, and renal function parameters were monitored at 7, 14, and 21 days of age. Two hundred one-day-old healthy male Avian broilers were divided into four groups, namely control group, AFB₁ group (0.3 mg/kg AFB₁), +Se group (0.4 mg/kg Se), and AFB₁+Se group (0.3 mg/kg AFB₁+0.4 mg/kg Se). Compared with that of the control group, the relative weight of kidney was increased in the AFB₁ group. There were no significant differences between the AFB₁+Se group and the control group. By histopathological observation, the renal epithelia were swelling and necrosis at 7 and 21 days of age. Ultrastructurally, the lipid droplets and expanded endoplasmic reticulum appeared in the plasma of epithelia cells in the AFB₁ group. Enlarged mitochondria with degenerated cristae were observed in the +Se group. Compared with the control group, the contents of serum creatinine and serum uric acid in the AFB₁ group were increased, while the activity of renal Na⁺-K⁺ ATPase was decreased. When 0.4 mg/kg selenium was added into the diet containing 0.3 mg/kg AFB₁, there were no obvious histological changes in the AFB₁+Se group, and the contents of the serum creatinine and serum uric acid contents and the activity of renal Na⁺-K⁺ ATPase were close to those in the control group. In conclusion, sodium selenite exhibited protective effects on AFB₁-induced kidney toxicity in broilers.

Loss of tooth or enamel is widespread in multiple mammal lineages. Although several studies have been reported, the evolutionary mechanisms of tooth / enamel loss are still unclear. Most previous studies have found that some tooth-related genes have been inactivated in toothless and / or enamel-less mammals, such as ENAM, ODAM, C4orf26, AMBN, AMTN, DSPP, etc. Here, we conducted evolutionary analyses on ACPT plays a key role in amelogenesis, to interrogate the mechanisms. We obtained the ACPT sequences from 116 species, including edentulous and enamel-less mammals, then evolutionary analyses were implemented. The results showed that variant ORF-disrupting mutations have been detected in ACPT coding region among nine edentulous baleen whales and three enamel-less taxa (pygmy sperm whale, aardvark, nine-banded armadillo). Furtherly, selective pressure uncovered that the selective constraints have been relaxed among all toothless and enamel-less lineages. Moreover, our results support the hypothesis that mineralized teeth were lost or degenerated in the common ancestor of crown Mysticeti through two shared single-base sites deletion in exon 4 and 5 of ACPT among all living baleen whales. D_N / d_S values on transitional branches were used to estimate ACPT inactivation times. In the case of aardvark, inactivation of ACPT was estimated at ~23.60-28.32 Ma, which is earlier than the oldest pangolin fossil time (Orycteropus minutus, ~19Ma), suggesting that ACPT inactivation may result in degeneration or loss of enamel. Conversely, the inactivation time of ACPT estimated in armadillo (~10.18-11.30 Ma) is later than the oldest fossil time, suggesting that inactivation of ACPT may result from degeneration or loss of enamel in these mammals. Our findings suggested that different mechanisms of degeneration of tooth / enamel might exist among toothless and enamel-less lineages during evolution. Our study further considered that ACPT is a novel gene for studying tooth evolution.