ABSTRACT
Disposal of plastic waste has become a widely discussed issue, due to the potential environmental impact of improper waste disposal. Polyethylene terephthalate (PET) packaging accounted for 44.7% of single-serve beverage packaging in the US in 2021, and 12% of global solid waste. A strategic solution is needed to manage plastic packaging solid waste. Major beverage manufacturers have pledged to reduce their environmental footprint by taking steps towards a sustainable future. The PET bottle has several properties that make it an environmentally friendly choice. The PET bottle has good barrier properties as its single-layer, mono-material composition allows it to be more easily recycled. Compared to glass, the PET bottle is lightweight and has a lower carbon footprint in production and transportation. With modern advancements to decontamination processes in the recycling of post-consumer recycled PET (rPET or PCR), it has become a safe material for reuse as beverage packaging. It has been 30 years since the FDA first began certifying PCR PET production processes as compliant for production of food contact PCR PET, for application within the United States. This article provides an overview of PET bottle-to-bottle recycling and guidance for beverage manufacturers looking to advance goals for sustainability.
ABSTRACT
Fibroblast growth factor-2 (FGF2) protects the heart from ischemia-reperfusion (I-R) injury via a vast network of protein kinases. In the heart, downstream effectors of these FGF2-triggered signals have not yet been identified. It is hypothesized that nitric oxide (NO) signaling and ATP-sensitive potassium (K(ATP)) channel activity are key effectors of protein kinases activated by FGF2-mediated cardioprotection. Hearts with a cardiac-specific overexpression of FGF2 (FGF2 Tg) were subjected to I-R injury in the absence or the presence of selective inhibitors of NO synthase (NOS) isoforms or sarcolemmal (sarcK(ATP)) and mitochondrial (mitoK(ATP)) K(ATP) channels. Multiple NOS isoforms are necessary for FGF2-mediated cardioprotection, and nitrite levels are significantly reduced in FGF2 Tg hearts upon inhibition of protein kinase C or mitogen-activated protein kinases. Likewise, sarcK(ATP) and mitoK(ATP) channels are important for cardioprotection elicited by endogenous FGF2. These findings suggest that FGF2-induced cardioprotection occurs via protein kinase-NOS pathways as well as K(ATP) channel activity.
