Research on mycotoxins now requires a systematic study of post-exposure organisms. In this study, the effects of aflatoxin B1 (AFB1) on biofluids biomarkers were examined with metabolomics and biochemical tests. The results showed that milk concentration of aflatoxin M1 changed with the addition or removal of AFB1. AFB1 significantly affected serum concentrations of superoxide dismutase (SOD) and malon dialdehyde (MDA), SOD/MDA, and the total antioxidant capacity. Significant differences of volatile fatty acids and NH3-N were detected in the rumen fluid. Eighteen rumen fluid metabolites, 11 plasma metabolites, and 9 milk metabolites were significantly affected by the AFB1. These metabolites are mainly involved in the pathway of amino acids metabolism. Our results suggest that not only is the study of macro-indicators (milk composition and production) important, but that more attention should be paid to micro-indicators (biomarkers) when assessing the risks posed by mycotoxins to dairy cows.

Pesticides are chemical or biological substances to control pests and protect the crop yield. Most pesticides suffering from large amounts of losses in the environment lead to damage of ecological systems and food pollution. To reduce their losses and increase the utilization rate, we have developed bioinspired mussel avermectin nanoparticles [P(St-MAA)-Av-Cat] with strong adhesion to crop foliage by the emulsion-solvent evaporation method and chemical modification. They were near spheres with a diameter of around 120 nm. They displayed remarkable high avermectin content of more than 50% (w/w) and presented excellent storage stability as well as continuous sustained release. The photosensitive avermectins loaded were highly improved against ultraviolet light. Meanwhile, the retention rate of P(St-MAA)-Av-Cat on the crop foliage surfaces was significantly increased. As a result, the indoor toxicity of P(St-MAA)-Av-Cat was highly enhanced. The adhesive property strongly depended upon the functional groups on the nanoparticle surface. The multimodal binding mode of P(St-MAA)-Av-Cat to the crop foliage surface resulted in stronger adhesion and a longer retention time.

Flaxseed is rich in α-linolenic acid (ALA) and can increase omega-3 polyunsaturated fatty acid in the milk of dairy cows. However, the response of rumen fermentation to different forms of flaxseed supplementation is unknown. This study aimed to investigate the effect of different forms of flaxseed on the fatty acid profile, fermentation, and composition of bacteria in the rumen of dairy cows. In total, 30 Holstein dairy cows were selected and randomly assigned into three groups (10/group). Cows were fed a basal diet (control check; CK) or basal diets supplemented with either 1,500 g per day whole flaxseed (WF) or 1,500 g per day ground flaxseed (GF). The WF group had the highest ALA content in rumen fluid, whereas no difference was found between the CK and GF groups. However, the molar proportion of acetate increased in the WF and GF groups and was the highest in the GF group, and a similar trend was shown by propionate, isobutyrate, butyrate, isovalerate, and valerate (CK < WF < GF). The abundance of Ruminococcaceae_NK4A214_group, Christensenellaceae_R-7_group, and Eubacterium_coprostanoligenes_group also showed the same trend (CK < WF < GF). Different forms of flaxseed release ALA by different mechanisms in the rumen, and the molar proportions of volatile fatty acids and the bacterial composition were potentially influenced mainly by the amount of ALA released into the rumen.

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The presence of mycotoxins in feed has the potential to cause significant detriment to animal and human health, and even severe economic implications. Previous studies on the effects of mycotoxins mainly focused on the addition of commercially available mycotoxins into feeds in animals. In the present study, corn meal and cottonseed were kept in warm and humid conditions to allow for mycotoxins produced and then used to substitute 50% and 100% of normal corn meal and cottonseed in diets for lactating cows for 14 days. The results showed that aflatoxin M1, deoxynivalenol, aflatoxin B1, and zearalenone were primary mycotoxins in milk from cows fed the diets. Compared with the control group, feeding the diets containing mildewy corn meal and cottonseed reduced feed intake, milk yield, and milk fat, protein and lactose productions (p > 0.05). No significant difference was observed in the acetate and valerate concentrations, acetate to propionate ratio, and the calculated CH4 production in rumen fluid (p > 0.05), whereas, the propionate, butyrate, isovalerate concentrations were affected (p < 0.05) depending on the content and type of natural mycotoxins. Serum creatinine and total glyceride concentrations were influenced with corn meal and cottonseed fully replaced with the mildewy feeds. Metabolic pathways for small molecule metabolites in milk were altered by dietary mycotoxin exposures, and the changes were mainly associated with amino acid metabolism, glucose metabolism, and energy metabolism. However, cows exposed to natural mycotoxins in the diets were still in healthy conditions and had low somatic cell count in milk.

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The t9,c12,c15-C18:3 as an isomer of α-linolenic acid (c9,c12,c15-C18:3; ALA), has been recently detected in milk, but has not been found in the rumen. This study hypothesized that it may be a biohydrogenation product of ALA in rumen and aimed to explore whether it was present in the rumen and help to understand the rumen biohydrogenation mechanisms of ALA. The in vitro experiment included two treatments, a control check (CK group) with 50 µL ethanol added, and ALA group with 50 µL ethanol and 2.6 mg ALA (ALA addition calculated by 1.30% of dry matter base of diet); each sample of fermentation fluid had the composition of C18 fatty acids analyzed at 0, 0.5, 1, 2, 3, 4, 5, and 6 h. The results showed that no t9,c12,c15-C18:3 was detected in the CK group, but ALA addition increased the concentration of t9,c12,c15-C18:3 in fermentation fluid. The content of t9,c12,c15-C18:3 peaked 1 h after fermentation, then declined gradually. At 1 h, no t9c12c15-C18:3 was detected in the fermentation fluid of the CK treatment. The results suggested that ALA converted to the isomer t9,c12,c15-C18:3 through biohydrogenation in the rumen. The addition of ALA can also increase the concentration of t9,c12-C18:2, c9,t11-C18:2, c12-C18:1, t11-C18:1, t9-C18:1, and c6-C18:1 in fermentation fluid. It was concluded using an in vitro experiment that t9,c12,c15-C18:3 was a product of rumen biohydrogenation of ALA.