Nutritional and environmental contributions to autism spectrum disorders: Focus on nutrigenomics as complementary therapy.

The prevalence of autism spectrum disorders (ASD) has risen sharply in the last 30 years, posing a major public health concern and a big emotional and financial challenge for families. While the underlying causes remain to be fully elucidated, evidence shows moderate genetic heritability contribution, but heavy environmental influence. Over the last decades, modern lifestyle has deeply changed our eating, rest, and exercise habits, while exposure to air, water, and food chemical pollution has increased due to indiscriminate use of pesticides, food additives, adjuvants, and antibiotics. The result is a drastic change in the quality of our energy source input, and an overload for antioxidant and detoxification pathways that compromises normal metabolism and homeostasis. Current research shows high prevalence of food selectivity and/or food allergy among children with autism, resulting in essential micronutrient deficits that may trigger or aggravate physical and cognitive symptoms. Nutrigenomics is an emerging discipline that focuses on genotype-micronutrient interaction, and a useful approach to tailor low risk, personalized interventions through diet and micronutrient supplementation. Here, we review available literature addressing the role of micronutrients in the symptomatology of ASD, the metabolic pathways involved, and their therapeutic relevance. Personalized and supervised supplementation according to individual needs is suggested as a complement of traditional therapies to improve outcome both for children with autism and their families.

Effects of sequential exposure to water accommodated fraction of crude oil and chlorpyrifos on molecular and biochemical biomarkers in rainbow trout.

Fish can be simultaneously or sequentially exposed to various kinds of pollutants, resulting in combined effects. Polycyclic aromatic hydrocarbons induce cytochrome P450 monooxygenase 1A (CYP1A) expression, which catalyzes the conversion of the organophosphorus insecticide chlorpyrifos (CPF) into its most active derivative, CPF-oxon. CPF-oxon inhibits CYP1A and other enzymes, including carboxylesterases (CEs) and acetylcholinesterase (AChE). We studied the effects of an in vivo exposure to crude oil water accommodated fraction (WAF) followed by an ex vivo exposure of liver tissue to CPF on the expression of Cyp1a, AhR and ARNT mRNA, CYP1A protein and on the activity of biomarker enzymes in the rainbow trout (Oncorhynchus mykiss). Juvenile rainbow trout were exposed to WAF (62 µg L-1 TPH) for 48 h. Then, liver was dissected out, sliced and exposed to 20 µg L-1 CPF ex vivo for 1 h. Liver tissue was analyzed for mRNA and protein expression and for CEs, AChE, glutathione S-transferase (GST) and CYP1A (EROD) activity. WAF induced Cyp1a mRNA and CYP1A protein expression by 10-fold and 2.5-8.3-fold, respectively, with no effect of CPF. WAF induced AhR expression significantly (4-fold) in control but not in CPF treated liver tissue. ARNT mRNA expression was significantly lowered (5-fold) by WAF. CPF significantly reduced liver EROD activity, independently of WAF pre-treatment. CEs activity was significantly inhibited in an additive manner following in vivo exposure to WAF (42%) and ex vivo exposure to CPF (19%). CPF exposure inhibited AChE activity (37%) and increased GST activity (42%).

Chemical characterization and toxicity of water-accommodated fraction of oil on the South American native species Hyalella curvispina.

Chemical and toxicological crude oil analysis was performed on water-accommodated fraction of oil (WAF). This study characterized the chemical composition of WAF and its dissipation over a period of 192 h. Acute (96 h) and chronic (14 d) toxicity of WAF were evaluated on Hyalella curvispina from both reference (Los Barreales lake, LB) and hydrocarbon-contaminated (Durán stream, DS) sites. The total hydrocarbon (TPHs) concentration in WAF was 2.18 mg L-1. The dissipation rates of hydrocarbons in WAF showed a first-order kinetics, with half-lives ranging between 65 h-200 h. Amphipods from LB showed acute and chronic LC50 values of 0.33 and 0.018 mg L-1, respectively. Amphipods from DS exposed to pure WAF showed no mortality in either acute or chronic assays. Further biochemical and molecular research is required to determine the mechanisms underlying the resistance to WAF exposure on DS amphipods.