Modified-masked T-2 toxin (mT-2) formed during metabolism in edible aquatic animals may go undetected by traditional analytical methods, thereby underestimating T-2 toxicity. The effects of T-2 on growth and antioxidant capacity and histopathological changes in the hepatopancreas were studied in Pacific white shrimp Litopenaeus vannamei exposed for 20 d to 0, 0.5, 1.2, 2.4, 4.8, and 12.2 mg/kg of T-2 in their feed. The concentration of mT-2 in the hepatopancreas was detected by liquid chromatography-tandem mass spectrophotometry before and after trifluoroacetic acid (TFA) treatment that converted mT-2 to free T-2. A dose-dependent increase in mT-2 concentration was observed in the hepatopancreas. Dietary exposure to T-2 significantly decreased (P < 0.05) shrimp growth and survival rate compared with the controls. The malondialdehyde (MDA) concentration was significantly increased in shrimp exposed to feed with ≥2.4 mg/kg T-2 (P < 0.05). The antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPx), total antioxidant capacity (T-AOC), and also glutathione (GSH) content increased in shrimp dosed with 2.4-4.8 mg/kg T-2 but declined at the highest dose (12.2 mg/kg), probably indicating an inability to cope with high concentrations of reactive oxygen species (ROS) as evident from a marked increase in MDA (P < 0.05) culminating in cellular toxicity. Histopathological changes in the hepatopancreas were dose dependent, with cell autophagy evident at the highest exposure dose. This is the first report in shrimp of a dose-dependent increase in ROS, SOD enzyme activity, and T-AOC at low T-2 exposures, and associated histopathological changes in the hepatopancreas, in response to dietary T-2. Received January 26, 2016; accepted October 9, 2016.
Brucellosis is a prevalent zoonotic disease worldwide. However, the spatiotemporal patterns evolution and its driving factors of Brucellosis have not been well explored. In this study, spatiotemporal scan statistics were applied to describe the spatiotemporal pattern of evolution in Brucellosis from 2003 to 2019 in mainland China, and GeoDetector analysis was further conducted to explore the driving effects of environmental, meteorological, and socioeconomic factors. We identified a distinct seasonal pattern for Brucellosis, with a peak in May and lowest incidence between September and December. High-risk clusters were first observed in the northwestern pastoral areas and later expanded to the southern urban areas. The spatiotemporal heterogeneity was mainly explained by total SO2 emissions, average annual temperature, sheep output, and consumption of meat per capita with explanatory powers of 45.38%, 44.60%, 40.76%, and 30.46% respectively. However, the explanatory power changed over time. Specifically, the explanatory power of average annual temperature tended to decrease over time, while consumption of meat per capita and total output of animal husbandry tended to increase. The most favorable conditions for the spread of Brucellosis include 0.66–0.70 million tons of SO2 emissions, 9.54–11.68 °C of average annual temperature, 63.28–72.40 million heads of sheep output, and 16.81–20.58 kg consumption of meat per capita. Brucellosis remains more prevalent in traditional pastoral areas in Northwest China, with the tendency of spreading from pastoral to non-pastoral, and rural to urban, areas. Total SO2 emission, average annual temperature, sheep output, and consumption of meat per capita dominated the spatial heterogeneity of Brucellosis with changes in explanatory power over time.
Mycotoxins are secondary metabolites produced by fungi. These contaminate dried seafoods during processing and storage and represent a potential health hazard for consumers. A sensitive, selective and accurate liquid chromatography/tandem mass spectrometry (LC-MS/MS) method was established for simultaneous quantification of four common mycotoxins (aflatoxin B1 (AFB1), T-2 toxin (T-2), ochratoxin A (OTA) and deoxynivalenol (DON)) in dried shrimp, dried fish and dried mussel products. Mycotoxins were extracted from dried seafood samples by acetonitrile/water (85/15, v/v), subjected to ultrasound for 60 min at 20 °C and cleaned up by defatting with n-hexane. The sample matrix affected the linearity of detection (R2 ≥ 0.9974). The limit of detection (LOD) and limit of quantification (LOQ) in dried seafood products varied from 0.1 to 2.0 µg·kg−1 and 0.3 to 5.0 µg·kg−1, respectively. The method was validated by spiking samples with specific mycotoxin levels, and the recoveries, intra-relative standard deviation (RSDs) and inter-RSDs ranged between 72.2–98.4%, 2.8–10.6%, and 5.5–15.4%, respectively. This method was used to analyze 40 dried seafood products purchased from the Zhanjiang seafood market. Results of this product sampling showed that while no DON was detected, AFB1, T-2 and OTA were detected in 30.8%, 17.5% and 33.3% of the samples, respectively. AFB1, T-2 and OTA concentrations varied at 0.58–0.89, 0.55–1.34 and 0.36–1.51 µg·kg−1, respectively. Relatively high frequency of contamination and the presence of AFB1, OTA and T-2 residues indicate the need to monitor mycotoxins in dried seafood products.
Vibrio parahaemolyticus (Vp), a major food-borne pathogen, is responsible for severe infections such as gastroenteritis and septicemia, which may be accompanied by lifethreatening complications. While studies have evaluated factors that affect the virulence of the pathogen, none have investigated the interaction of Vp with gut microbiota. To address this knowledge gap, we compared the effect of Vp on gut bacterial community structure, immunity, liver and kidney function, in pseudo germ-free (PGF) mice and normal (control) mice. Significant damage to the ileum was observed in normal mice compared with the PGF mice. The inflammatory factors IL-1β, IL-6, and TNF-α in normal mice were ∼2.5-fold higher than in the PGF mice, and liver (ALT, AST, ALP) and kidney (BUN) function indices were ∼1.6-fold higher. The Vp infection substantially reduced species composition and richness of the gut microbial communities. In particular, there was a shift in keystone taxa, from protective species of genera Bacteroides, Lactobacillus, Bifidobacterium, and Akkermansia in the gut of control mice to opportunistic pathogens Enterobacteriaceae, Proteus, Prevotella, and Sutterella in Vp-infected mice, thus affecting microbiota-related biological functions in the mice. Specifically, pathways involved in infectious diseases and ion channels were significantly augmented in infected mice, while the pathways involved in metabolism, digestion and cell growth declined. We propose that the normal mice are more prone to Vp infection because of the alteration in gut-microbe-mediated functions. All these effects reduce intestinal resistance, with marked damage to the gut lining and pathogen leakage into the blood culminating in liver and kidney damage. These findings greatly advance our understanding of the mechanisms underlying interactions between Vp, the gut microbiota and the infected host.
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