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Since environmental effects of molecular traits are often questioned we analyze here the molecular effects of cadmium (Cd) on lipid pathways and their effects on tissues development. Lipids are an important energy source for the developing embryo, and accumulate in the ovary and hepatopancreas of decapod crustaceans. The extend of Cd affecting lipid storage and metabolism, is studied here with the freshwater crabs Sinopotamon henanense. Crabs were exposed to water-born Cd at 1.45, 2.9, 5.8 mg/l for 10, 15, and 20 days. With significantly increased Cd accumulation in exposed crabs, lipid content in hepatopancreas and ovary showed a time-dependent and concentration-dependent reduction, being at least one of the reasons for a lower ovarian index (OI) and hepatopancreatic index (HI). After 10-day exposure increased triglyceride (TG) level in hemolymph and up-regulation of pancreatic lipase (PL) activity in the hepatopancreas suggested an increased nutritional lipid uptake. However, two processes led to lower lipid levels upon Cd exposure: an increased utilization of lipids and a down-regulated lipoprotein lipase (LPL) led to insufficient lipid transport. 10-day Cd exposure also triggered the production of β-nicotinamide adenine dinucleotide 2'-phosphate reduced tetrasodium salt hydrate (NADPH), as well as to the synthesis of adenosine triphosphate (ATP) and fatty acids. With increasing exposure time, the crabs at 15 and 20-day exposure contained less lipid and TG, suggesting that more energy was consumed during the exposure time. Meanwhile, the level of NADPH, ATP and the activity of PL, LPL, fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) activity was down-regulated suggesting an impairment of the crab metabolism by Cd in addition to causing a lower lipid level. [ABSTRACT FROM AUTHOR]

Since environmental effects of molecular traits are often questioned we analyze here the molecular effects of cadmium (Cd) on lipid pathways and their effects on tissues development. Lipids are an important energy source for the developing embryo, and accumulate in the ovary and hepatopancreas of decapod crustaceans. The extend of Cd affecting lipid storage and metabolism, is studied here with the freshwater crabs Sinopotamon henanense. Crabs were exposed to water-born Cd at 1.45, 2.9, 5.8 mg/l for 10, 15, and 20 days. With significantly increased Cd accumulation in exposed crabs, lipid content in hepatopancreas and ovary showed a time-dependent and concentration-dependent reduction, being at least one of the reasons for a lower ovarian index (OI) and hepatopancreatic index (HI). After 10-day exposure increased triglyceride (TG) level in hemolymph and up-regulation of pancreatic lipase (PL) activity in the hepatopancreas suggested an increased nutritional lipid uptake. However, two processes led to lower lipid levels upon Cd exposure: an increased utilization of lipids and a down-regulated lipoprotein lipase (LPL) led to insufficient lipid transport. 10-day Cd exposure also triggered the production of β-nicotinamide adenine dinucleotide 2'-phosphate reduced tetrasodium salt hydrate (NADPH), as well as to the synthesis of adenosine triphosphate (ATP) and fatty acids. With increasing exposure time, the crabs at 15 and 20-day exposure contained less lipid and TG, suggesting that more energy was consumed during the exposure time. Meanwhile, the level of NADPH, ATP and the activity of PL, LPL, fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) activity was down-regulated suggesting an impairment of the crab metabolism by Cd in addition to causing a lower lipid level. [ABSTRACT FROM AUTHOR]