Alginate Encapsulation Stabilizes Xylanase Toward the Laccase Mediator System.

Xylanase, a hydrolytic enzyme, is susceptible to inactivation by the oxidative conditions generated by the laccase mediator system (LMS). Given the impetus to develop a mixed enzyme system for application in biomass processing industries, xylanase was encapsulated with either Cu2+- or Ca2+-alginate and then exposed to the LMS with variations such as mediator type, mediator concentration, and treatment pH. Results demonstrate that alginate-encapsulated xylanase retains substantial activity (> 80%) when exposed to the LMS relative to non-encapsulated xylanase. Cu2+-alginate generally provided better protection than Ca2+-alginate for all mediators, and protection was observed even at a low pH, where the LMS is most potent. Despite encapsulation, xylanase was still capable of hydrolyzing its polymeric substrate xylan, given kcat/Km values within an order of magnitude of that for non-encapsulated xylanase. The alginate matrix does not impede the function of the oxidized mediator, since comparable Vmax values were observed for the conversion of veratryl alcohol to veratraldehyde by free and Cu2+-alginate encapsulated laccase. Overall, these results support development of a mixed enzyme system for biomass delignification and, more broadly, show potential for protecting protein function in an oxidative environment.

Counteracting Environmental Chemicals with Coenzyme Q10: An Educational Primer for Use with "Antioxidant CoQ10 Restores Fertility by Rescuing Bisphenol A-Induced Oxidative DNA Damage in the Caenorhabditis elegans Germline".

Environmental toxicants are chemicals that negatively affect human health. Although there are numerous ways to limit exposure, the ubiquitous nature of certain environmental toxicants makes it impossible to avoid them entirely. Consequently, scientists are continuously working toward developing strategies for combating their harmful effects. Using the nematode Caenorhabditis elegans, a model with many genetic and physiological similarities to humans, researchers in the Colaiácovo laboratory have identified several molecular mechanisms by which the toxic agent bisphenol A (BPA) interferes with reproduction. Here, we address their recent discovery that a widely available compound, Coenzyme Q10 (CoQ10), can rescue BPA-induced damage. This work is significant in that it poses a low-cost method for improving reproductive success in humans. The goal of this primer is to assist educators and students with navigating the paper entitled "Antioxidant CoQ10 Restores Fertility by Rescuing Bisphenol A-Induced Oxidative DNA Damage in the Caenorhabditis elegans Germline." It is ideally suited for integration into an upper-level undergraduate course such as Genetics, Cell and Molecular Biology, Developmental Biology, or Toxicology. The primer provides background information on the history of BPA, the utility of the C. elegans germ line as a model for studying reproductive toxicity, and research methods including assessment of programmed cell death, fluorescent microscopy applications, and assays to quantify gene expression. Questions for deeper exploration in-class or online are provided.Related article in GENETICS: Hornos Carneiro MF, Shin N, Karthikraj R, Barbosa F Jr, Kannan K, Colaiácovo MP. Antioxidant CoQ10 restores fertility by rescuing bisphenol A-induced oxidative DNA damage in the Caenorhabditis elegans Germline. Genetics 214:381-395.

Neonicotinoid-containing insecticide disruption of growth, locomotion, and fertility in Caenorhabditis elegans.

Neonicotinoids, a class of insecticides structurally similar to nicotine that target biting and sucking insects, are the most widely used insecticides today, in part due to their supposed low toxicity in other organisms. However, a growing body of research has found that even low doses of neonicotinoids can induce unexpected negative effects on the physiology and survival of a wide range of non-target organisms. Importantly, no work has been done on the commercial formulations of pesticides that include imidacloprid as the active ingredient, but that also contain many other components. The present study examines the sublethal effects of "Tree and Shrub"™ ("T+S"), a commercial insecticide containing the neonicotinoid imidacloprid as its active ingredient, on Caenorhabditis elegans. We discovered that "T+S" significantly stunted the overall growth in wildtype nematodes, an effect that was exacerbated by concurrent exposure to heat stress. "T+S" also negatively impacted fecundity as measured by increased germline apoptosis, a decrease in egg-laying, and fewer viable offspring. Lastly, exposure to "T+S" resulted in degenerative changes in nicotinic cholinergic neurons in wildtype nematodes. As a whole, these findings demonstrate widespread toxic effects of neonicotinoids to critical functions in nematodes.