Silkie (SK) chickens, valued for dark meat, serve as a model to study melanin deposition in muscle. Integrated transcriptomics and metabolomics of SK vs. Arbor Acres (AA) broiler pectoralis were used to identify key molecular drivers of meat color. All birds were cage-raised under standardized temperature and light conditions with free access to feed and water. Pectoralis muscle samples were collected from 24-day-old healthy SK and AA chickens (n = 6). Transcriptome profiling identified 488 differentially expressed genes in SK chickens, with seven conserved melanogenesis genes (TYRP1, MLANA, TYR, MLPH, EDNRB2, PMEL, GPNMB) consistently upregulated across dark-pectoralis breeds, and melanogenesis and WNT pathways were activated. Co-expression network analysis highlighted SOX10 as a key hub regulator. Metabolomics quantified 129 differentially abundant metabolites. A critical finding was the significant depletion of L-tyrosine and its derivatives in SK muscle, despite upregulated melanogenesis genes. It indicates intense metabolic flux toward pigment synthesis. Integrated analyses converged on tyrosine metabolism and redox pathways: oxidized glutathione and p-coumaric acid correlated negatively with pigment deposition, while ADP-ribose and pyridoxal correlated positively. Additionally, novel inhibitors PNMT and HIBADH may modulate melanin deposition. These findings reveal a trade-off between pigment deposition and redox balance, providing molecular markers for poultry melanin-related trait improvement.

Chronic cyclic heat stress impairs thermoregulation, growth, tissue integrity, microbial metabolism, and stress-related molecular responses in broiler chickens. N-acetyl-L-cysteine, a cysteine donor involved in glutathione synthesis, has been proposed as a nutritional strategy to support stress adaptation. Therefore, this study evaluated NAC in 324 Ross 308 broilers allocated to thermoneutral conditions (TN, 7 pens), HS (HS, 10 pens), or HS plus 2000 mg/kg NAC (HS + NAC, 10 pens). From day 20 to 35, HS birds were exposed to 34 °C for 7 h/day and 26 °C otherwise, while TN birds were kept at 22 °C. Heat stress increased rectal temperature and respiratory rate (p < 0.001), reduced average daily gain, and increased drinking and gasping behavior (p < 0.05). Heat stress also increased hepatic cord disorganization, cerebral vacuolisation–necrocytosis, hepatic and cerebral HSP70 expression, and caecal propionate, while reducing cerebral apelin expression (p < 0.05). Jejunal villus morphology and microbiota α-diversity were unchanged, although caecal profiles indicated treatment-related shifts and potentially higher Bilophila spp. in heat-stressed birds. NAC did not improve growth, thermoregulation, oxidative status, caecal fermentation, microbial structure, or HSP70 expression. It increased jejunal villus fusion and hepatocellular vacuolation scores and reduced cerebral ghrelin expression (p < 0.05). In conclusion, heat stress impaired growth and induced tissue, microbial, fermentative, and cerebral gene-expression changes, whereas 2000 mg/kg NAC did not provide measurable protection under the chronic cyclic HS in the present study.