Cerebral gene expression in response to single or combined gestational exposure to methylmercury and selenium through the maternal diet

Controversy remains regarding the safety of consuming certain types of seafood, particularly during pregnancy. While seafood is rich in vital nutrients, it may also be an important source of environmental contaminants such as methylmercury (MeHg). Selenium (Se) is one essential element present in seafood, hypothesised to ameliorate MeHg toxicity. The aim of the present study was to ascertain the impact of Se on MeHg-induced cerebral gene expression in a mammalian model. Microarray analysis was performed on brain tissue from 15-day-old mice that had been exposed to MeHg throughout development via the maternal diet. The results from the microarray analysis were validated using qPCR. The exposure groups included: MeHg alone (2.6 mg kg−1), Se alone (1.3 mg kg−1), and MeHg + Se. MeHg was presented in a cysteinate form, and Se as Se–methionine, one of the elemental species occurring naturally in seafood. Eight genes responded to Se exposure alone, five were specific to MeHg, and 63 were regulated under the concurrent exposure of MeHg and Se. Significantly enriched functional classes relating to the immune system and cell adhesion were identified, highlighting potential ameliorating mechanisms of Se on MeHg toxicity. Key developmental genes, such as Wnt3 and Sparcl1, were also identified as putative ameliorative targets. This study, utilising environmentally realistic forms of toxicants, delivered through the natural route of exposure, in association with the power of transcriptomics, highlights significant novel information regarding putative pathways of selenium and MeHg interaction in the mammalian brain

Dietary fatty acids and inflammation in the vertebral column of Atlantic salmon, Salmo salar L., smolts : a possible link to spinal deformities

Vegetable oils (Vo) are an alternative to fish oil (Fo) in aquaculture feeds. This study aimed to evaluate the effect of dietary soybean oil (Vo diet), rich in linoleic acid, and of dietary fish oil (Fo diet) on the development of spinal deformities under bacterial lipopolysaccharide (LPS)-induced chronic inflammation conditions in Atlantic salmon, Salmo salar L. Fish [25 g body weight (BW)] were fed the experimental diets for 99 days. On day 47 of feeding (40 g BW), fish were subjected to four experimental regimes: (i) intramuscular injections with LPS, (ii) sham-injected phosphate-buffered saline (PBS), (iii) intraperitoneally injected commercial oil adjuvant vaccine, or (iv) no treatment. The fish continued under a common feeding regime in sea water for 165 more days. Body weight was temporarily higher in the Vo group than in the Fo group prior to immunization and was also affected by the type of immunization. At the end of the trial, no differences were seen between the dietary groups. The overall prevalence of spinal deformities was approximately 14% at the end of the experiment. The Vo diet affected vertebral shape but did not induce spinal deformities. In groups injected with LPS and PBS, spinal deformities ranged between 21% and 38%, diet independent. Deformed vertebrae were located at or in proximity to the injection point. Assessment of inflammatory markers revealed high levels of plasma prostaglandin E-2 (PGE(2)) in the Vo-fed and LPS-injected groups, suggesting an inflammatory response to LPS. Cyclooxigenase 2 (COX-2) mRNA expression in bone was higher in fish fed Fo compared to Vo-fed fish. Gene expression of immunoglobulin M (IgM) was up-regulated in bone of all LPS-injected groups irrespective of dietary oil. In conclusion, the study suggests that Vo is not a risk factor for the development of inflammation-related spinal deformities. At the same time, we found evidence that localized injection-related processes could trigger the development of vertebral body malformations

Dietary phosphorus does not reduce the risk for spinal deformities in a model of adjuvant-induced inflammation in Atlantic salmon (Salmo salar) postsmolts

Inflammation is a non-specific protective mechanism towards injury known to affect bone remodelling. This study aimed to investigate the effect of Freunds complete adjuvant (FCA) induced-inflammation on the prevalence of spinal deformities of Atlantic salmon postsmolts fed with two different dietary P levels. Sextuple groups of salmon postsmolts were fed with either a low-phosphorous (6 g kg-1 available P, LP) or a high-phosphorous (9 g kg-1 available P) diet for a period of 101 days. On Day 102, individually tagged fish were subjected to (i) single injection with FCA (0.125 mg kg-1 BW) dissolved in phosphate-buffered saline (PBS) (ii) placebo injection with PBS or (iii) sham injection (insertion of needle only) or (iv) remained untreated. On Day 103, fish were given a common diet for 174 days in seawater. No significant differences in body weight were observed. Injected fish, particularly the FCA group, had more compressions in the injection site than untreated fish. No effect of diet and no interaction between treatment and diet were observed. Severe scoliosis was observed in similar to 7% of FCA-injected individuals, corresponding to a mixture of bone malformations in the tail region. In conclusion, experimentally induced inflammation may be an independent risk factor for bone deformities in Atlantic salmon