Polyphenol-enriched azuki bean (Vina angularis) extract reduces the oxidative stress and prevents DNA oxidation in the hearts of streptozotocin-induced early diabetic rats.

We examined the changes in the heart of rats at the early stages of streptozotocin (STZ)-induced diabetes, and whether azuki bean extract (ABE) could influence these changes. The experimental diabetic rats received 0 or 40 mg/kg of ABE orally for 4 weeks, whereas the control group rats received distilled water. 8-Hydroxy-2'-deoxyguanosine (8-OHdG) and expression of proteins associated with peroxisomal FA ß-oxidation as well as oxidative stress markers were examined. The levels of peroxisomal ACOX1 and catalase of the diabetic groups were significantly higher than those in the control group. The levels of p62, phosphorylated-p62 (p-p62) and HO-1 in the STZ group were significantly higher than those in the control group, and the levels of p-p62, HO-1, and 8-OHdG were significantly lower by ABE administration. The STZ-induced early diabetes increases the levels of proteins related to peroxisomal FA ß-oxidation and oxidative stress markers in hearts. ABE protects diabetic hearts from oxidative damage.

Changes in liver PPARalpha mRNA expression in response to two levels of high-safflower-oil diets correlate with changes in adiposity and serum leptin in rats and mice.

The ligand-dependent transcription factor peroxisome proliferator-activated receptor alpha (PPARalpha) is known to be activated by common fatty acids and to regulate the expression of genes of various lipid oxidation pathways and transport. High-fat diets provide more fatty acids, which presumably could enhance lipid catabolism through up-regulation of PPARalpha signaling. However, high intake of fat could also lead to obesity. To examine PPARalpha signaling in high-fat feeding and obesity, this study examined the hepatic mRNA expression of PPARalpha and some of its target genes in Wistar rats and C57BL/6J mice fed two levels (20% or 30% wt/wt) of high-safflower-oil (SFO; oleic-acid-rich) diets until animals showed significantly higher body weight (13 weeks for rats and 22 weeks for mice) than those of control groups fed a 5% SFO diet. At the end of these respective feeding periods, only the rats fed 30% SFO and the mice fed 20% SFO among the two groups fed high-fat diets showed significantly higher body weight, white adipose tissue weight, serum leptin and mRNA expression of PPARalpha (P<.05) compared to the respective control groups. Despite elevated acyl-CoA (a PPARalpha target gene) protein and activity in both groups fed high-fat diets, the mRNA expression level of most PPARalpha target genes examined correlated mainly to PPARalpha mRNA levels and not to fat intake or liver lipid levels. The observation that the liver PPARalpha mRNA expression in groups fed high-fat diets was significantly higher only in obese animals with elevated serum leptin implied that obesity and associated hyperleptinemia might have a stronger impact than dietary SFO intake per se on PPARalpha-regulated mRNA expression in the liver.

Signs of recovery of mussels health two years after the Prestige oil spill.

To assess the biological effects of the Prestige oil spill (November 2002) on coastal ecosystems, mussels (Mytilus galloprovincialis) were sampled in 22 locations along the coast of Galicia and the Bay of Biscay in April, July and September 2003 and in February, April, July and October 2004. Several cell and tissue-level biomarkers were measured in digestive gland. Flesh condition index and gamete development stages were assessed as supporting parameters. AOX activity, a marker of exposure to peroxisome proliferating compounds including PAHs, was particularly low in Galicia in 2003 and further was markedly increased in several localities in 2004. Values of the labilization period (LP) of the lysosomal membrane were low in all the studied localities, especially in Galicia in 2003. In 2004, LP values raised, evidencing a certain recovery in mussel's health. In agreement, the volume density of basophilic cells was markedly high in 2003 and showed a decreasing trend throughout 2004. Parameters defining the structure of digestive alveoli showed few variations between 2003 and 2004. Significant correlations between several biomarkers and total polycyclic aromatic hydrocarbons (PAHs) were found. In conclusion, employed biomarkers detected highest degree of disturbance in areas most impacted by the oil spill (Galicia) and were able to evidence a recovery trend during 2004, related to a decrease in total PAH concentrations in mussels.

Specificity of the peroxisome proliferation response in mussels exposed to environmental pollutants.

Peroxisome proliferation has been proposed as novel biomarker of exposure to organic pollutants in aquatic organisms. Peroxisome proliferator compounds comprise a heterogeneous group of substances known for their ability to cause massive proliferation of peroxisomes and liver carcinogenesis in sensitive species such as rodents. Recently, several marine organisms (mussels and fish) have been shown as target species of peroxisome proliferators. In the present work, we aimed to investigate the specificity of the peroxisome proliferation response in mussels. For this purpose, mussels (Mytilus edulis) were exposed for three weeks to North Sea crude oil (NSO), a mixture of NSO, alkylphenols and extra PAHs (MIX), diallylphthalate (DAP), bisphenol-A (BPA) and tetrabromodiphenylether (TBDE), or transplanted for three weeks to four stations showing different copper concentrations in a copper mine. Peroxisome proliferation was assessed by measuring the activity of the peroxisomal beta-oxidation enzyme acyl-CoA oxidase (AOX) and the volume density occupied by peroxisomes (V(VP)) in the digestive gland. Mussels exposed to NSO and MIX showed significantly increased AOX activities and V(VP) compared to control animals. Significantly higher V(VP) was also found in DAP and TBDE exposed mussels. V(VP) did not vary in mussels transplanted into a copper concentration gradient. Our results confirm the usefulness and specificity of peroxisome proliferation as a suitable biomarker of exposure to organic contaminants such as oil derived hydrocarbons, phthalate plasticizers and polybrominated flame retardants in mussels.