This study aimed to find the SNPs in the SORBS1 gene of cattleyak, analyze the relationship between its polymorphisms and the milk fat traits, and find potential molecular markers for the milk fat traits of cattleyak. The polymorphism of the SORBS1 gene in 350 cattleyak from Hongyuan County (Sichuan, China) were detected by PCR and DNA sequencing, and the correlation between these SNPs and the milk production traits of cattleyak was analyzed. The results showed that there were nine SNPs in the CDS and their adjacent non-coding regions of the SORBS1 gene, and all SNPs have three genotypes. The correlation analysis found that the genotypes with superior milk fat traits in the other eight alleles were homozygous genotypes with a high genotype frequency except the g.96284 G > A (c.3090 G > A) (p < 0.05). However, at locus g.96284 G > A, the milk fat percentage, monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs) and saturated fatty acids (SFAs) of the GA genotype were significantly higher than that of GG and AA genotypes (p < 0.05). Among these SNPs, three SNPs (g.6256 C > T (c.298 C > T), g.24791 A > G (c.706 A > G) and g.29121 A > G (c.979 A > G)) caused the amino acids change. The genotypes of the three SNPs consist of three haplotypes and four diplotypes. The amino acid mutation degree of diplotype H1–H1 (CCAAAA) was the highest, and its milk fat percentage, MUFAs, PUFAs and SFAs were also the highest (p < 0.05). Taken together, we found nine SNPs in the SORBS1 gene that are closely related to the milk fat traits of cattleyak. Moreover, the mutation of amino acids caused by SNPs had positive effects on the milk fat traits of cattleyak. H1-H1 is the dominant diplotype which significantly related to the milk fat traits of cattleyak. This study provides a new molecular marker and theoretical basis for screening the milk fat traits of cattleyak.

Zearalenone (ZEN), a mycotoxin, is toxic to skeletal muscle, and the solution to alleviate its damage remains unknown. Here, we analyzed the toxic effect of ZEN on muscle and the mitigation of antioxidants (GSH, NMN, and melatonin) for this toxicity. The results showed that 0.02 mmol/L ZEN inhibited myoblast viability and myogenic differentiation, accompanied by reducing Type I and Type IIA and increasing Type IIX myofibers. Antioxidants (NMN with 0.5 mmol/L, GSH with 1 mmol/L, and melatonin with 1 mmol/L) rescued these phenotypes. Mice that were delivered 3 mg/kg body weight (BW)/day of ZEN by gavage for 35 days exhibited a similar trend of muscle fiber composition, but the gavage of antioxidants (NMN with 500 mg/kg BW/day, GSH with 300 mg/kg BW/day, and melatonin with 100 mg/kg BW/day) abolished this phenotype. Mechanistically, ZEN treatment increased ROS production, resulting in oxidative stress, mitochondrial dysfunction, and, subsequently, myofiber changes. Additionally, ZEN indirectly contributed to its damage, decreasing the abundance of Lactobacillus at the genus level and increasing Streptococcus sp. at the species level, which was associated with lactic acid production. Antioxidants partially rescued this microbiota composition. This study explores ZEN toxicity effects and alleviation of antioxidants, which provides new insights and attenuation solutions for ZEN damage to skeletal muscle. However, the underlying molecular mechanism of ZEN and antioxidants in the skeletal muscle still needs to be explored.