Volumen 6 (2022): Edición 2 (April 2022)

Trolox (6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid) is a highly hydrophilic α-tocopherol analog that is widely used as a standard against which the antioxidant ability of other chemicals is measured and represented in Trolox equivalents. However, the effect of pH values on the hydroxyl radical scavenging activity has not been fully studied yet. In this study, the HOO^• antiradical activity of Trolox in water was studied. It was found that the H-abstraction of the O1-H bond determined the activity of the neutral and monoanion states, whereas the electron transfer reaction of the hydroxyl anion state determined the activity of the dianion state. Although the total rate constant increased following the increase in pH levels, the overall rate constant of the Trolox + HOO^• reaction in water changed when pH levels rose due to the decrease in HOO^• molar fraction. The results also revealed that at pH < 2, the O1-radical was the main intermediate of the Trolox + HOO^• reaction in water, whereas, at pH ---gt--- 5, the anion-radical was the significant intermediate. Thus the rate constants and the reaction intermediates vary with the pH values.

Background: Industrial Biotechnology (“White Biotechnology”) is the large-scale production of materials and chemicals using renewable raw materials along with biocatalysts like enzymes derived from microorganisms or by using microorganisms themselves (“whole cell biocatalysis”). While the production of ethanol has existed for several millennia and can be considered a product of Industrial Biotechnology, the application of complex and engineered biocatalysts to produce industrial scale products with acceptable economics is only a few decades old. Bioethanol as fuel, lactic acid as food and PolyHydroxyAlkanoates (PHA) as a processible material are some examples of products derived from Industrial Biotechnology.

Purpose and Scope: Industrial Biotechnology is the sector of biotechnology that holds the most promise in reducing our dependence on fossil fuels and mitigating environmental degradation caused by pollution, since all products that are made today from fossil carbon feedstocks could be manufactured using Industrial Biotechnology – renewable carbon feedstocks and biocatalysts. To match the economics of fossil-based bulk products, Industrial Biotechnology-based processes must be sufficiently robust. This aspect continues to evolve with increased technological capabilities to engineer biocatalysts (including microorganisms) and the decreasing relative price difference between renewable and fossil carbon feedstocks. While there have been major successes in manufacturing products from Industrial Biotechnology, challenges exist, although its promise is real. Here, PHA biopolymers are a class of product that is fulfilling this promise.

Summary and Conclusion: The authors illustrate the benefits and challenges of Industrial Biotechnology, the circularity and sustainability of such processes, its role in reducing supply chain issues, and alleviating societal problems like poverty and hunger. With increasing awareness among the general public and policy makers of the dangers posed by climate change, pollution and persistent societal issues, Industrial Biotechnology holds the promise of solving these major problems and is poised for a transformative upswing in the manufacture of bulk chemicals and materials from renewable feedstocks and biocatalysts.

Genetically modified mice are engineered as models for human diseases. These mouse models include inbred strains, mutants, gene knockouts, gene knockins, and ‘humanized’ mice. Each mouse model is engineered to mimic a specific disease based on a theory of the genetic basis of that disease. For example, to test the amyloid theory of Alzheimer’s disease, mice with amyloid precursor protein genes are engineered, and to test the tau theory, mice with tau genes are engineered. This paper discusses the importance of mouse models in basic research, drug discovery, and translational research, and examines the question of how to define the “best” mouse model of a disease. The critiques of animal models and the caveats in translating the results from animal models to the treatment of human disease are discussed. Since many diseases are heritable, multigenic, age-related and experience-dependent, resulting from multiple gene-gene and gene-environment interactions, it will be essential to develop mouse models that reflect these genetic, epigenetic and environmental factors from a developmental perspective. Such models would provide further insight into disease emergence, progression and the ability to model two-hit and multi-hit theories of disease. The summary examines the biotechnology for creating genetically modified mice which reflect these factors and how they might be used to discover new treatments for complex human diseases such as cancers, neurodevelopmental and neurodegenerative diseases.

There are several possible ways to measure the contraction of cells in vitro. Here, we report measurements of the contractile properties of 3T3-L1 cells grown to confluence on 3D hollow capsules. The capsules were fabricated using the layer-by-layer polyelectrolyte deposition technique on a polymer core. After the polyelectrolyte film was completed, the core was dissolved to leave the hollow capsule. The contractile force of the cells was determined from the deformation in the capsule size induced by interruption of the actin cytoskeleton of the cells that adhered to the outer surface of the hollow capsules, using prior measurements of the elastic modulus of the capsule. From the measurements of the compressive modulus for the capsules (of 6.52 μN), those capsule deformations indicate that the forskolin relaxed the layer of cells by 19.6 μN and the cytochalasin-D relaxed the layer of cells by 45.6 μN. The density of cells in the layer indicated that the force associated with the forskolin-induced relaxation of a single cell is 3.2 nN and the force associated with the cytochalasin-D-induced relaxation of a single cell is 7.5 nN. The mechanism of action of forskolin through second messenger pathways to disrupt the assembly of actin stress fibres also explains its reduced effect on cell contraction compared to that for cytochalasin-D, which is a compound that directly inhibits the polymerization of F-actin filaments.