Impact of Multiple Reprocessing on Properties of Polyhydroxybutyrate and Polypropylene.

Biobased plastics have the potential to be sustainable, but to explore their circularity further, current end-of-life options need to be broadened. Mechanical recycling is one of the most accepted methods to bring back plastics into the loop. Polyhydroxybutyrates (PHBs) are biobased and biodegradable in nature with promising properties and varied applications in the market. This study focuses on their potential for mechanical recycling by multiple extrusion cycles (E1-E5) and multi-faceted characterization of the virgin (V) and reprocessed materials from E1 to E5. The behavior is compared to polypropylene (PP) as a reference with a similar property profile, which has also been reprocessed five times. The thermal properties of both series showed a stable melting point and thermal decomposition temperature from thermal analyses (differential scanning calorimetry (DSC) and thermogravimetric analysis (TGA)). However, a steady increase in the degree of crystallinity was observed which could counterbalance the decrease in molecular weight due to repeated extrusion measured by gel permeation chromatography and resulted in similar values of tensile strength across the cycles. The strain at break was impacted after the first extrusion, but no significant change was observed thereafter; the same was observed for impact strength. Even in scanning electron microscopy (SEM) images, virgin and E5 samples appeared similar, showing the stability of morphological characteristics. Fourier transform infrared spectroscopy (FTIR) results revealed that no new groups are being formed even on repeated processing. The deviation between the PHB and PP series was more predominant in the melt mass flow rate (MFR) and rheology studies. There was a drastic drop in the MFR values in PHB from virgin to E5, whereas not much difference was observed for PP throughout the cycles. This observation was corroborated by frequency sweeps conducted with the parallel plate method. The viscosity dropped from virgin to E1 and E2, but from E3 to E5 it presented similar values. This was in contrast to PP, where all the samples from virgin to E5 had the same values of viscosity. This paper highlights the possibilities of mechanical recycling of PHB and explains why future work with the addition of virgin material and other additives is an area to be explored.

Bile acid-induced apoptosis in hepatocytes is caspase-6-dependent.

Apoptosis induced by hydrophobic bile acids is thought to contribute to liver injury during cholestasis. Caspase-6 is an executioner caspase that also appears to have regulatory functions in hematopoetic cell lines. We aimed to elucidate the role of caspase-6 in bile acid-induced apoptosis. The major human hydrophobic bile acid, glycochenodeoxycholic acid (GCDCA, 75 micromol/liter), rapidly induced caspase-6 cleavage in HepG2-Ntcp human hepatoma cells. GCDCA-induced, but not tumor necrosis factor alpha- or etoposide-induced activation of effector caspases-3 and -7 was significantly reduced by 50% in caspase-6-deficient HepG2-Ntcp cells as well as in primary rat hepatocytes pretreated with a caspase-6 inhibitor. Inhibition of caspase-9 reduced GCDCA-induced activation of caspase-6, whereas inhibition of caspase-6 reduced activation of caspase-8 placing caspase-6 between caspase-9 and caspase-8. GCDCA also induced apoptosis in Fas-deficient Hep3B-Ntcp and HuH7-Ntcp hepatoma cells. In addition, GCDCA-induced apoptosis was reduced by 50% in FADD-deficient HepG2-Ntcp cells, whereas apoptosis induced by tumor necrosis factor alpha was reduced by 90%. Collectively, these observations suggest that GCDCA can induce hepatocyte apoptosis in the absence of death receptor signaling, presumably by a compensatory mitochondrial pathway. In conclusion, caspase-6 appears to play an important regulatory role in the promotion of bile acid-induced apoptosis as part of a feedback loop.

Free fatty acids sensitize hepatocytes to bile acid-induced apoptosis.

Delivery of free fatty acids to the liver in nonalcoholic fatty liver disease (NAFLD) may render hepatocytes more vulnerable to glycochenodeoxycholic acid (GCDCA)-induced apoptosis. Fat overloading was induced in HepG2-Ntcp cells and primary rat hepatocytes by incubation with palmitic or oleic acid. Apoptosis was quantified by measuring caspase 3/7 activity and transcription of interleukin (IL) 8 and IL-22 by quantitative real-time PCR. Oleic acid (500 microM) alone did not induce apoptosis, while palmitic acid (500 microM) increased apoptosis 5-fold. GCDCA did not induce significant apoptosis at low micromolar concentrations (5-30 microM) in non-steatotic cells. However, at the same concentrations, GCDCA increased apoptosis 3-fold in oleic acid-pretreated HepG2-Ntcp cells and 3.5-fold in primary rat hepatocytes. Pretreatment with oleic acid increased GCDCA-induced gene transcription of the proinflammatory cytokines IL-8 and IL-22 5-fold and 19-fold, respectively. Thus, low levels of cholestasis normally not considered harmful could advance liver injury in patients with NAFLD.