Photosynthetic conversion of carbon dioxide from cement production to microalgae biomass.

Production of microalgae is a potential technology for capturing and recycling carbon dioxide from cement kiln emissions. In this study, a process of selecting a suitable strain that would effectively utilize carbon dioxide and generate biomass was investigated. A down-selection screening method was applied to 28 strains isolated from the area surrounding a commercial cement plant. In laboratory-scale (1 L) continuous-mode chemostats, observed productivity was > 0.9 g L-1 d-1 for most strains studied. Chlorella sorokiniana (strain SMC-14M) appeared to be the most tolerant to cement kiln gas emissions in situ, delivered under control of a pH-stat system, and was down-selected to further investigate growth and biomass production at large-scale (1000 L) cultivation. Results demonstrated little variability in lipid, crude protein, and carbohydrate composition throughout growth between kiln-gas grown algal biomass and biomass produced with laboratory grade CO2. The growth rate at which the maximum quantity of CO2 from the emissions is recycled also produced the maximum amount of the targeted biomass components to increase commercial value of the biomass. An accumulation of some heavy metals throughout its growth demonstrates the necessity to monitor the biomass cultivated with industrial flue gases and to carefully consider the potential applications for this biomass; despite its other attractive nutritional properties. KEY POINTS: • Studied high biomass producing algal strains grown on CO2 from cement flue gas. • Chlorella sorokiniana SMC-14M grew well at large scale, in situ on cement flue gas. • Demonstrated the resulting commercial potential of the cultured algal biomass.

A Rat Study to Evaluate the Protein Quality of Three Green Microalgal Species and the Impact of Mechanical Cell Wall Disruption.

The present study was conducted to evaluate the protein quality of microalgae species Chlorella vulgaris (CV), Chlorella sorokiniana (CS), and Acutodesmus obliquus (AO) and assess the impact of mechanical cell wall disruption. Male Sprague-Dawley rats, around 156 g after adaptation, were placed in metabolic cages and fed experimental diets that were either protein-free or contained 10% protein solely from one of the undisrupted or disrupted CV, CS, and AO. After 3 days, feces were collected for a period of 5 days and analyzed together with diet samples for crude protein contents. Apparent protein digestibility, true protein digestibility, amino acid score, and protein digestibility-corrected amino acid score were calculated. In vitro protein digestibility was measured using the pepsin-pancreatin method and the in vitro protein digestibility-corrected amino acid score was calculated. The crude protein contents of CV, CS, and AO were 53.5, 50.2, and 40.3%, respectively. The amino acid score of the first limiting amino acid was 1.10, 1.27, and 0.86, true protein digestibility was 64.7, 59.3, and 37.9% and protein digestibility-corrected amino acid score was 0.63, 0.64, and 0.29, respectively, for CV, CS, and AO. Mechanical cell disruption significantly improved protein digestibility without a substantial impact on the amino acid profile and score, resulting in the increase of protein digestibility-corrected amino acid score to 0.77, 0.81, and 0.46, respectively, for disrupted CV, CS, and AO. There was a strong correlation between in vitro protein digestibility and apparent protein digestibility (r = 0.986), and also between in vitro protein digestibility-corrected amino acid score and in vivo protein digestibility-corrected amino acid score (r = 0.994). The results suggest that the CV and CS are acceptable sources of protein for humans and animals and quality can be markedly improved by mechanical cell wall disruption. Additionally, in vitro protein digestibility measured using the pepsin-pancreatin method may be used to screen protein product candidates, save animals, reduce cost, and accelerate product development.

Biogeography of resistance to paralytic shellfish toxins in softshell clam, Mya arenaria (L.), populations along the Atlantic coast of North America.

Blooms of Alexandrium spp., the causative agent of paralytic shellfish poisoning (PSP), recur with varying frequency and intensity on the Northwest Atlantic coast of North America, from New York, USA, to northern Canadian waters. Along this latitudinal range blooms co-occur with abundant, intertidal populations of softshell clams, Mya arenaria. Prior work identified a naturally-occurring genetic mutation in Domain II α-subunit of the clams' voltage-gated sodium channels (NaV), which significantly reduces the binding affinity of the paralytic shellfish toxin, saxitoxin (STX). This mutation provides clams with resistance to the deleterious effects of STX, allowing them to continue feeding during Alexandrium spp. blooms and attain very high tissue toxicities. This study used genetic sequencing of the NaV mutation locus in clams from four coastal regions of the Bay of Fundy-Gulf of Maine and the mid-Atlantic to determine the percentage of clams in each region that possess the resistant NaV mutation. The genotype composition was related to the occurrence and magnitude of PSP outbreaks based on shellfish toxicity, primarily that of mussels, Mytilus edulis, used as a proxy for the prevalence and severity of Alexandrium blooms in each region. As hypothesized, the proportion of clams bearing the resistant mutation generally matched up well with the historical incidence and intensity of Alexandrium spp. blooms. The highest percentage of homozygote resistant clams (RR = 70.0%), and the lowest percentage of sensitive clams (SS = 4.5%) were found in eastern Gulf of Maine populations. Exceptions at a few sites where anomalously high numbers of M. arenaria with the resistant mutation were found despite the absence of blooms, may be attributable to larval gene flow. There was no evidence that Alexandrium blooms occurring in Northport Harbor, Long Island, have resulted in a shift in genotypic composition of the local clam population, presumably due to their low cell toxicity. Seasonal mismatch of highly vulnerable M. arenaria postset with toxic blooms at this latitude may also partly explain this result. This study provides strong supporting evidence that Alexandrium blooms can select for resistance to PSP-toxins in M. arenaria populations and proposes a mechanism for the persistence of the sensitive allele throughout the region. Implications for clam aquaculture (seeding) efforts, as well as for shellfish toxicity monitoring are discussed.

Maximizing the productivity of the microalgae Scenedesmus AMDD cultivated in a continuous photobioreactor using an online flow rate control.

In this study, production of the microalga Scenedesmus AMDD in a 300 L continuous flow photobioreactor was maximized using an online flow (dilution rate) control algorithm. To enable online control, biomass concentration was estimated in real time by measuring chlorophyll-related culture fluorescence. A simple microalgae growth model was developed and used to solve the optimization problem aimed at maximizing the photobioreactor productivity. When optimally controlled, Scenedesmus AMDD culture demonstrated an average volumetric biomass productivity of 0.11 g L-1 d-1 over a 25 day cultivation period, equivalent to a 70 % performance improvement compared to the same photobioreactor operated as a turbidostat. The proposed approach for optimizing photobioreactor flow can be adapted to a broad range of microalgae cultivation systems.

Sodium channel mutation leading to saxitoxin resistance in clams increases risk of PSP.

Bivalve molluscs, the primary vectors of paralytic shellfish poisoning (PSP) in humans, show marked inter-species variation in their capacity to accumulate PSP toxins (PSTs) which has a neural basis. PSTs cause human fatalities by blocking sodium conductance in nerve fibres. Here we identify a molecular basis for inter-population variation in PSP resistance within a species, consistent with genetic adaptation to PSTs. Softshell clams (Mya arenaria) from areas exposed to 'red tides' are more resistant to PSTs, as demonstrated by whole-nerve assays, and accumulate toxins at greater rates than sensitive clams from unexposed areas. PSTs lead to selective mortality of sensitive clams. Resistance is caused by natural mutation of a single amino acid residue, which causes a 1,000-fold decrease in affinity at the saxitoxin-binding site in the sodium channel pore of resistant, but not sensitive, clams. Thus PSTs might act as potent natural selection agents, leading to greater toxin resistance in clam populations and increased risk of PSP in humans. Furthermore, global expansion of PSP to previously unaffected coastal areas might result in long-term changes to communities and ecosystems.