75 Effects of endophyte-infected tall fescue on performance of genotyped pregnant beef cows and heifers supplemented with rumen-protected niacin

Abstract

Abstract Fescue toxicity is the result of cattle consuming fungal (Ergot spp.) endophyte tall fescue, a perennial forage widely used in the United States. Ergot alkaloids produce vasoconstriction; however, rumen-protected Niacin (RPN), known by its vasodilation ability, may act as an alleviator for fescue toxicity. Our objective was to assess the effects of a genetic test for fescue toxicity susceptibility, and RPN supplementation on animal performance, hepatic gene expression, and uterine arteries blood flow of Angus × Simmental pregnant animals consuming endophyte-infected tall fescue seeds. Ninety days prior to calving, genotyped pregnant cows (n = 11) and heifers (n = 17) were stratified by body weight (BW; 540 ± 207 kg) and genetic resistance to fescue toxicity (susceptible or tolerant); and randomly assigned to dietary treatments: 1) Susceptible Control (SC); 2) Susceptible Niacin (SN); 3) Tolerant Control (TC); and 4) Tolerant Niacin (TN). Animals’ BW and liver samples were obtained on days 0 and 29. Uterine arteries blood flow was measured using Doppler ultrasonography on treatment days 3, 10, 17, and 23. Messenger RNA was extracted from liver samples for RT-qPCR. Gene expression and BW data were analyzed using the PROC MIXED procedure of SAS, and uterine arteries blood flow was analyzed with the GLIMMIX procedure of SAS. Between day 0 and 29, SOD1 and CYP2E1 were upregulated (P < 0.05) in TC and SC, respectively. Furthermore, SOD2 expression in SC was significantly lower (P < 0.05) on day 29. Genetic test and RPN did not affect uterine arteries’ blood flow. TN animals had a greater decrease in BW compared with other treatments (P < 0.01). In conclusion, Doppler ultrasonography did not detect any changes in uterine arteries blood flow and, supplementation with RPN may influence the oxidative status of cows’ liver consuming endophyte-infected fescue seeds.