Does titanium in ionic form display a tissue-specific distribution?

Most studies have focused on the biodistribution of titanium(IV) oxide as nanoparticles or crystals in organism. But several reports suggested that titanium is released from implant in ionic form. Therefore, gaining insight into toxicokinetics of Ti ions will give valuable information, which may be useful when assessing the health risks of long-term exposure to titanium alloy implants in patients. A micro synchrotron radiation-induced X-ray fluorescence (µ-SRXRF) was utilized to investigate the titanium distribution in the liver, spleen and kidneys of rats following single intravenous or 30-days oral administration of metal (6 mg Ti/b.w.) in ionic form. Titanium was mainly retained in kidneys after both intravenous and oral dosing, and also its compartmentalization in this organ was observed. Titanium in the liver was non-uniformly distributed—metal accumulated in single aggregates, and some of them were also enriched in calcium. Correlation analysis showed that metal did not displace essential elements, and in liver titanium strongly correlated with calcium. Two-dimensional maps of Ti distribution show that the location of the element is characteristic for the route of administration and time of exposure. We demonstrated that µ-SRXRF can provide information on the distribution of titanium in internal structures of whole organs, which helps in enhancing our understanding of the mechanism of ionic titanium accumulation in the body. This is significant due to the popularity of titanium implants and the potential release of metal ions from them to the organism

Resolvin D2 plays a protective role in RAW 264.7 Cells treated with polycyclic aromatic hydrocarbons

Eicosanoids are signaling molecules that control the immune processes and might have effects on inflammatory diseases. The aim of our study was to evaluate the effect of added resolvin D2 (RvD2), after treatment with polycyclic aromatic hydrocarbons (PAHs), on RAW 264.7 cells by using a UHPLC/MS-TOF method for the quantification of eicosanoids: 8-iPGF3α, PGF3α, 8-isoPGF2α, PGF2α and 5-iPF2α as well as cyclooxygenase 2 (COX-2), prostaglandin E synthase (cPGES) and prostaglandin F2α (FP) receptor protein expression by Western blot. The levels of PGF3α, PGF2α 8-iPGF3α 8-isoPGF2α and 5-iPF2α were decreased in RAW 264.7 cells after the exposure to PAHs and treatment with RvD2. It was observed that COX-2, cPGES and FP-receptor expression was decreased after co-treatment of the cells with PAHs and RvD2. Our findings suggest that RvD2 has anti-oxidant, anti-inflammatory and pro-resolving properties that may contribute significantly to alleviation of the harmful effects caused by PAHs in macrophages. Moreover, these results suggest that a diet rich in n-3 fatty acids might be helpful in resolving the inflammation and mitigating the effects of environmental stress in macrophages

Testing of triglyceride rich lipoproteins oxidative susceptibility

Lipoproteiny bogatotriglicerydowe (ang.: Triglyceride Rich Lipoprotein, TRL) oraz podwyższony poziom ich remnantów są znacząco powiązane z chorobami układu sercowo- naczyniowego. Adult Treatment Panel III, zestaw zasad diagnostyki dyslipidemii dorosłych i Narodowy Program Cholesterolowy (NCEP) wprowadził definicje nowych odmian dyslipidemii doceniając rolę sprawczą triglicerydów w miażdżycy i patogenezie zespołu metabolicznego. Oksydacyjne modyfikacje lipoprotein o niskiej gęstości (LDL) są uznanym testem diagnostycznym tej kategorii aterogennych lipoprotein znanym i powszechnie stosowanym od wielu lat. Nowością jest zainteresowanie modyfikacją oksydacyjną lipoprotein bogatotriglicerydowych. W niniejszej pracy uzyskano obrazy krzywych kinetycznych oksydacji klasycznej frakcji LDL cholesterolu oraz frakcji nie HDL-cholesterolu. W przypadku LDL stężenie jonów miedzi było determinantą przyrostu produktu – oksydowanych lipidów w czasie (TBARS) i klasycznego trójfazowego lub nie przebiegu krzywej. Analiza pól powierzchni pod krzywymi kinetycznymi oksydacji jak i wartości maksymalnej uzyskanego produktu oraz lag fazy potwierdza fakt, że w zastosowanych modelach to stężenie białka a nie stężenie użytego oksydanta decyduje o przebiegu krzywej, podatności lipoprotein nie-HDL na oksydację i trójfazowym przebiegu krzywej oraz obecności lag fazy pozwalającej na wyznaczenie dodatkowego parametru diagnostycznego – oporności frakcji na oksydację. Analizy oksydacji TRL sugerują złożone zależności modyfikacji oksydacyjnej składników surowicy, zapewne interakcje pomiędzy lipidami i białkami, z udziałem puli kwasów tłuszczowych i endogennych antyoksydantów liofilowych i hydrofilowych. Analiza ta poszerza możliwości szacowania czynników progresji miażdżycy.Triglyceride Rich Lipoprotein (TRL) and increased level of their remnants are highly correlated with cardio-vascular diseases. Adult Treatment Panel III and National Cholesterol Education Program introduced new definitions of hyperlipidemic state related to the triglyceride atherogenic potency. LDL oxidative modification was tested in the context of their atherogenicity from many years. Quite new topic is the TRL oxidation. In this work the kinetics of LDL and non-HDL cholesterol (TRL) fraction oxidation was investigated. In the LDL oxidation model the concentration of oxidant – copper ion is considered a determinant of the kinetic curve shape. Analysis of area under kinetic curve of non-HDL lipoprotein oxidation revealed that the protein component is the main determinant of TRL oxidative susceptibility and resistance. This study confirmed the complexity of the TRL oxidative response and its relevance to potential prognostic marker for atherosclerosis