Impact of COVID-19 on the indigenous population of Brazil: a geo-epidemiological study.

This study aimed to analyse the geographical distribution of coronavirus disease 2019 (COVID-19) and to identify high-risk areas in space and time for the occurrence of cases and deaths in the indigenous population of Brazil. This is an ecological study carried out between 24 March and 26 October 2020 whose units of analysis were the Special Indigenous Sanitary Districts. The Getis-Ord General G and Getis-Ord Gi* techniques were used to verify the spatial association of the phenomena and a retrospective space-time scan was performed. There were 32 041 confirmed cases of COVID-19 and 471 deaths. The non-randomness of cases (z score = 5.40; P < 0.001) and deaths (z score = 3.83; P < 0.001) were confirmed. Hotspots were identified for cases and deaths in the north and midwest regions of Brazil. Sixteen high-risk space-time clusters were identified for the occurrence of cases with a higher RR = 21.23 (P < 0.001) and four risk clusters for deaths with a higher RR = 80.33 (P < 0.001). These clusters were identified from 22 May and were active until 10 October 2020. The results indicate critical areas in the indigenous territories of Brazil and contribute to better directing the actions of control of COVID-19 in this population.

Improving pollutants environmental risk assessment using a multi model toxicity determination with in vitro, bacterial, animal and plant model systems: The case of the herbicide alachlor.

Several environmental pollutants, including pesticides, herbicides and persistent organic pollutants play an important role in the development of chronic diseases. However, most studies have examined environmental pollutants toxicity in target organisms or using a specific toxicological test, losing the real effect throughout the ecosystem. In this sense an integrative environmental risk of pollutants assessment, using different model organisms is necessary to predict the real impact in the ecosystem and implications for target and non-target organisms. The objective of this study was to use alachlor, a chloroacetanilide herbicide responsible for chronic toxicity, to understand its impact in target and non-target organisms and at different levels of biological organization by using several model organisms, including membranes of dipalmitoylphosphatidylcholine (DPPC), rat liver mitochondria, bacterial (Bacillus stearothermophilus), plant (Lemna gibba) and mammalian cell lines (HeLa and neuro2a). Our results demonstrated that alachlor strongly interacted with membranes of DPPC and interfered with mitochondrial bioenergetics by reducing the respiratory control ratio and the transmembrane potential. Moreover, alachlor also decreased the growth of B. stearothermophilus and its respiratory activity, as well as decreased the viability of both mammalian cell lines. The values of TC50 increased in the following order: Lemna gibba < neuro2a < HeLa cells < Bacillus stearothermophilus. Together, the results suggest that biological membranes constitute a putative target for the toxic action of this lipophilic herbicide and point out the risks of its dissemination on environment, compromising ecosystem equilibrium and human health.

Safety of Yam-Derived (Dioscorea rotundata) Foodstuffs-Chips, Flakes and Flour: Effect of Processing and Post-Processing Conditions.

The production of yam-derived (Dioscorea rotundata) foodstuffs is mainly performed by small and medium scale processors that employ old traditional methods. This can lead to differences in quality from processor to processor, and from location to location, with consequent safety concerns. As such, the effects of processing and post-processing phases (i.e., storage, transport, etc.) on the safety of some yam-derived foodstuffs-namely chips, flakes, and flour-has been evaluated, with a focus on bacterial and fungal contamination, aflatoxins, pesticides, and heavy metals (Pb, Ni, Cd and Hg). Yams harvested and processed in Nigeria were screened, being that the country is the largest producer of the tuber, with 70⁻75% of the world production. Results highlighted no presence of pesticides, however, many samples showed high levels of bacterial and fungal contamination, together with heavy metal concentrations above the recommended safety levels. No trend was observed between the items considered; it was noticed, however, that samples purchased from the markets showed higher contamination levels than those freshly produced, especially regarding bacterial and aflatoxins presence. The processing stage was identified as the most critical, especially drying. Nonetheless, post-processing steps such as storage and handling at the point of sale also contributed for chemical contamination, such as aflatoxin and heavy metals. The results suggested that both the processing and post-processing phases have an impact on the safety of yam chips, flakes, and flour.

Toxicity of the herbicide linuron as assessed by bacterial and mitochondrial model systems.

Linuron is one of the most intensively used herbicides with predictable effects on the environment and non-target organisms. In the present study, two in vitro biological models (a Bacillus sp. and rat liver mitochondria) were used to evaluate linuron toxicity at a cell/subcellular level. Linuron inhibited bacterial growth and NADH-supported respiration, similar IC50 values being estimated for both toxic responses (74 and 98 µM, respectively). At concentrations up to 120 µM, linuron perturbed the respiration and phosphorylation efficiency of rat liver mitochondria, reflected by an increase of state 4 respiration and a decrease of the transmembrane potential, state 3 and FCCP-uncoupled respiration, when malate/glutamate or succinate were used as respiratory substrates. Consequently, a decrease of the respiratory control and ADP/O ratio was observed. This study suggests that linuron membrane interactions with adverse repercussions in the activity of membrane enzymatic complexes, such as those which constitute the prokaryotic and mitochondrial respiratory systems, may underlie the toxic effects exerted by that herbicide on non-target organisms. Moreover, this work contributes to the establishment of our bacterial model system as a good tool for chemical toxicity screening.

Interaction of fullerene nanoparticles with biomembranes: from the partition in lipid membranes to effects on mitochondrial bioenergetics.

Partition and localization of C60 and its derivative C60(OH)18-22 in lipid membranes and their impact on mitochondrial activity were studied, attempting to correlate those events with fullerene characteristics (size, surface chemistry, and surface charge). Fluorescence quenching studies suggested that C60(OH)18-22 preferentially populated the outer regions of the bilayer, whereas C60 preferred to localize in deeper regions of the bilayer. Partition coefficient values indicated that C60 exhibited higher affinity for dipalmitoylphosphatidylcholine and mitochondrial membranes than C60(OH)18-22. Both fullerenes affected the mitochondrial function, but the inhibitory effects promoted by C60 were more pronounced than those induced by C60(OH)18-22 (up to 20 nmol/mg of mitochondrial protein). State 3 and p-trifluoromethoxyphenylhydrazone-uncoupled respirations are inhibited by both fullerenes when glutamate/malate or succinate was used as substrate. Phosphorylation system and electron transport chain of mitochondria are affected by both fullerenes, but only C60 increased the inner mitochondrial membrane permeability to protons, suggesting perturbations in the structure and dynamics of that membrane. At concentrations of C60(OH)18-22 above 20 nmol/mg of mitochondrial protein, the activity of FoF1-ATP synthase was also decreased. The evaluation of transmembrane potential showed that the mitochondria phosphorylation cycle decreased upon adenosine diphosphate addition with increasing fullerenes concentration and the time of the repolarization phase increased as a function of C60(OH)18-22 concentration. Our results suggest that the balance between hydrophilicity and hydrophobicity resulting from the surface chemistry of fullerene nanoparticles, rather than the cluster size or the surface charge acquired by fullerenes in water, influences their membrane interactions and consequently their effects on mitochondrial bioenergetics.

Studies on the toxicity of an aqueous suspension of C60 nanoparticles using a bacterium (gen. Bacillus) and an aquatic plant (Lemna gibba) as in vitro model systems.

The increasing use of C60 nanoparticles and the diversity of their applications in industry and medicine has led to their production in a large scale. C60 release into wastewaters and the possible accumulation in the environment has raised concerns about their ecotoxicological impact. In the present study, an aqueous suspension of C60 nanoparticles was prepared and its potential toxicity studied in laboratory, using a bacterium (Bacillus stearothermophilus) and an aquatic plant (Lemna gibba) as model systems. C60 nanoparticles inhibited the growth of L. gibba, in contrast to that of the bacterium. Consistently, the ultrastructure and respiratory activity of bacterial cells were not affected by C60, but the contents of chlorophylls a and b and chloroplast oxygen production decreased considerably in L. gibba. Altogether, our results suggest that C60 aqueous dispersions must be viewed as an environmental pollutant, potentially endangering the equilibrium of aquatic ecosystems.

Unaltered hepatic oxidative phosphorylation and mitochondrial permeability transition in wistar rats treated with nimesulide: Relevance for nimesulide toxicity characterization.

Nonsteroidal anti-inflammatory drugs have been associated with hepatotoxicity in susceptible patients. One such example is nimesulide, a preferential cyclooxygenase 2-inhibitor, widely used for the treatment of inflammation and pain. It was suggested that nimesulide could exert its hepatotoxicity by altering hepatic mitochondrial function, which was demonstrated in vitro. The objective of this study was to verify whether liver mitochondria isolated from rats treated with doses of nimesulide well above therapeutic levels possessed decreased calcium tolerance and oxidative phosphorylation, which indicates in vivo nimesulide mitochondrial toxicity. Male and female rats received nimesulide or its vehicle twice daily, for 5 days, and were killed on the seventh day for the isolation of liver mitochondria. Mitochondrial respiration, transmembrane electric potential, and calcium tolerance were characterized in all experimental groups. Nimesulide had no effect on liver mitochondrial function. Indexes of mitochondrial integrity, calcium loading capacity, and oxidative phosphorylation efficiency were unchanged between liver mitochondria from treated and control animals. In the animals tested, no evidence of degraded mitochondrial function due to nimesulide administration could be found. The results corroborate the notion that despite recognized in vitro mitochondrial toxicity, nimesulide does not cause detectable mitochondrial dysfunction in Wistar rats, even when administered in much higher concentrations than those known to have anti-inflammatory effects.