Integrated genome-transcriptome analysis unveiled the mechanism of Debaryomyces hansenii-mediated arsenic stress amelioration in rice.

Globally, rice is becoming more vulnerable to arsenic (As) pollution, posing a serious threat to public food safety. Previously Debaryomyces hansenii was found to reduce grain As content of rice. To better understand the underlying mechanism, we performed a genome analysis to identify the key genes in D. hansenii responsible for As tolerance and plant growth promotion. Notably, genes related to As resistance (ARR, Ycf1, and Yap) were observed in the genome of D. hansenii. The presence of auxin pathway and glutathione metabolism-related genes may explain the plant growth-promoting potential and As tolerance mechanism of this novel yeast strain. The genome annotation of D. hansenii indicated that it contains a repertoire of genes encoding antioxidants, well corroborated with the in vitro studies of GST, GR, and glutathione content. In addition, the effect of D. hansenii on gene expression profiling of rice plants under As stress was also examined. The Kyoto Encyclopedia of Genes and Genomes (KEGG) database revealed 307 genes, annotated in D. hansenii-treated rice, related to metabolic pathways (184), photosynthesis (12), glutathione (10), tryptophan (4), and biosynthesis of secondary metabolite (117). Higher expression of regulatory elements like AUX/IAA and WRKY transcription factors (TFs), and defense-responsive genes dismutases, catalases, peroxiredoxin, and glutaredoxins during D. hansenii+As exposure was also observed. Combined analysis revealed that D. hansenii genes are contributing to stress mitigation in rice by supporting plant growth and As-tolerance. The study lays the foundation to develop yeast as a beneficial biofertilizer for As-prone areas.

Mitigation of arsenic toxicity in rice by the co-inoculation of arsenate reducer yeast with multifunctional arsenite oxidizing bacteria.

The study aimed to explicate the role of microbial co-inoculants for the mitigation of arsenic (As) toxicity in rice. Arsenate (AsV) reducer yeast Debaryomyces hansenii NBRI-Sh2.11 (Sh2.11) with bacterial strains of different biotransformation potential was attempted to develop microbial co-inoculants. An experiment to test their efficacy (yeast and bacterial strains) on plant growth and As uptake was conducted under a stressed condition of 20 mg kg-1 of arsenite (AsIII). A combination of Sh2.11 with an As(III)-oxidizer, Citrobacter sp. NBRI-B5.12 (B5.12), resulted in ∼90% decrease in grain As content as compared to Sh2.11 alone (∼40%). Reduced As accumulation in rice roots under co-treated condition was validated with SEM-EDS analysis. Enhanced As expulsion in the selected combination under in vitro conditions was found to be correlated with higher As content in the soil during their interaction with plants. Selected co-inoculant mediated enhanced nutrient uptake in association with better production of indole acetic acid (IAA) and gibberellic acid (GA) in shoot, support microbial co-inoculant mediated better biomass under stressful condition. Boosted defense response in association with enhanced glutathione-S-transferase (GST) and glutathione reductase (GR), activities under in vitro and in vivo conditions were observed. These results indicated that the As(III) oxidizer-B5.12 accelerated the As detoxification property of the As(V) reducer-Sh2.11. Henceforth, the results confer that the coupled reduction-oxidation process of the co-inoculant reduces the accumulation of As in rice grain. These co-inoculants can be further developed for field trials to achieve higher biomass with alleviated As toxicity in rice.

Luis Prunés Risetti: un gran maestro de la dermatología chilena: su biografía y archivo fotográfico / Luis Prunés Risetti: a great master of Chilean dermatology: his biography and photo archive

El doctor Luis Prunés fue uno de los grandes maestros de la dermatología chilena. Se formó como dermatólogo en el hospital Saint-Louis en París. En la década 1920 ingresó al Hospital San Luis de Santiago y en 1938 asumió como profesor titular de la cátedra “Clínica Universitaria de Piel y Sífilis” del Hospital San Vicente de Paul. En 1938 fue el primer presidente de la Sociedad Chilena de Dermato-sifilología. Fue un gran investigador de patologías cutáneas; estudió principalmente la lepra y las lesiones cutáneas asociadas a minerales. Es recordado por preconizar la importancia de la biopsia cutánea. Jubiló en 1954 dejándonos un importante legado dermatológico. El Dr. Prunés recopiló sus mejores casos en más de 20archivos fotográficos, los cuales se encuentran en la biblioteca del Departamento de Dermatología del Hospital Clínico de la Universidad de Chile. El objetivo de este trabajo es presentar parte de su archivo fotográfico, mostrando imágenes impresionantes de tumores cutáneos y lesiones cutáneas inducidas por arsénico.

Dr. Luis Prunés is one of the masters of the Chilean dermatology. He was trained as dermatologist at the Saint-Louis hospital in Paris. Since 1920 he worked as dermatologist at the San Luis Hospital in Santiago and in 1938 he took over as Professor and Chairman of the “University Clinic of Skin and Syphilis” at San Vicente de Paul Hospital. In 1938, he was the first president of the Chilean Society of Dermatology. He studied leprosy and skin lesions associated with minerals. He is also remembered for advocating the importance of skin biopsy. He retired in 1954, leaving an important legacy. Dr. Prunés compiled his best clinical cases in more than 20 photographic archives, which are located at the Library of the Dermatology Department in the University of Chile Clinical Hospital. The purpose of this paper is to present part of his photographic archive, showing stunning images of large cutaneous tumors and arsenic-induced skin lesions.

Arsenic accumulation in lichens of Mandav monuments, Dhar district, Madhya Pradesh, India.

Total arsenic in four different growth forms of lichens growing on old monuments in the city of Mandav, Dhar district of Madhya Pradesh, India was analyzed. Among the different growth forms, foliose lichens were found to accumulate higher amounts of arsenic followed by leprose form. The squamulose and crustose form accumulates the lower concentration of arsenic and ranged between 0.46 +/- 0.03 and 20.99 +/- 0.58 mircog g(-1) dry weight, while the foliose and leprose lichens have ranges from 10.98-51.95 and 28.63-51.20 mircog g(-1) dry weight, respectively. The substrate having high arsenic ranges also exhibit higher ranges of arsenic on lichens growing on them. The cyanolichens exhibit higher concentration of arsenic than the green photobiont-containing squamulose form. The higher concentration of arsenic was found at site having past mining activities. LSD (1%) shows significant difference for As concentration in lichens thallus between the selected sites and species both.

Pathogenesis, clinical features and pathology of chronic arsenicosis.

Arsenicosis is a multisystem disorder, with virtually no system spared from its vicious claw; though its predominant manifestations are linked to cutaneous involvement. Cutaneous effects take the form of pigmentary changes, hyperkeratosis, and skin cancers (Bowen's disease, squamous cell carcinoma, and basal cell epithelioma). Peripheral vascular disease (blackfoot disease), hypertension, ischemic heart disease, noncirrhotic portal hypertension, hepatomegaly, peripheral neuropathy, respiratory and renal involvement, bad obstetrical outcome, hematological disturbances, and diabetes mellitus are among the other clinical features linked to arsenic toxicity. The effects are mediated principally by the trivalent form of arsenic (arsenite), which by its ability to bind with sulfhydryl groups present in various essential compounds leads to inactivation and derangement of body function. Though the toxicities are mostly linked to the trivalent state, arsenic is consumed mainly in its pentavalent form (arsenate), and reduction of arsenate to arsenite is mediated through glutathione. Body attempts to detoxify the agent via repeated oxidative methylation and reduction reaction, leading to the generation of methylated metabolites, which are excreted in the urine. Understandably the detoxification/bio-inactivation process is not a complete defense against the vicious metalloid, and it can cause chromosomal aberration, impairment of DNA repair process, alteration in the activity of tumor suppressor gene, etc., leading to genotoxicity and carcinogenicity. Arsenic causes apoptosis via free radical generation, and the cutaneous toxicity is linked to its effect on various cytokines (e.g., IL-8, TGF-beta, TNF-alpha, GM-CSF), growth factors, and transcription factors. Increased expression of cytokeratins, keratin-16 (marker for hyperproliferation) and keratin-8 and -18 (marker for less differentiated epithelial cells), can be related to the histopathological findings of hyperkeratosis and dysplastic cells in the arsenicosis skin lesion.

Arsenicosis: diagnosis and treatment.

Diagnosis of arsenicosis relies on both clinical and laboratory criteria, but principally it can be diagnosed on the basis of its cutaneous manifestations. Cutaneous manifestations (melanosis, keratosis, and cutaneous cancers) are essential clues in the diagnosis, and trained dermatologists or arsenic experts are able to clinically confirm a case even without laboratory backup. Although systemic manifestations are not considered as diagnostic hallmarks, yet their presence serves as important telltale signs in arriving at the diagnosis. In countries where laboratory facilities are available, measuring the level of arsenic in drinking water (consumed in the last 6 months), urine, hair, and nails is of immense value. Newer biomarkers of arsenic exposure are being explored to provide early information about arsenic intoxication, of which urinary porphyrin level, blood metallothionein have shown promising results. Controlling the problem of arsenicosis depends on various factors, of which the most important is cessation of intake of arsenic-contaminated water. Deep wells, traditional dug wells, treatment of surface water, rainwater harvesting, and removing arsenic from the contaminated water by arsenic removal plant or arsenic treatment unit are the available options for providing arsenic-free drinking water. The role of nutrition and antioxidants in preventing the onset of symptoms of arsenicosis is also of importance. Nonspecific therapies (e.g., keratolytics for hyperkeratosis) cannot also be ignored and serve as palliative measures. The persons affected need to be followed up at regular intervals to detect the onset of cancers (if any) at the earliest. Role of counseling and education should never be underestimated since absence of public awareness can undermine all efforts of mitigation measures.

Epidemiology and prevention of chronic arsenicosis: an Indian perspective.

Arsenicosis is a global problem but the recent data reveals that Asian countries, India and Bangladesh in particular, are the worst sufferers. In India, the state of West Bengal bears the major brunt of the problem, with almost 12 districts presently in the grip of this deadly disease. Recent reports suggest that other states in the Ganga/Brahmaputra plains are also showing alarming levels of arsenic in ground water. In West Bengal, the majority of registered cases are from the district of Nadia, and the maximum number of deaths due to arsenicosis is from the district of South 24 Paraganas. The reason behind the problem in India is thought to be mainly geogenic, though there are instances of reported anthropogenic contamination of arsenic from industrial sources. The reason for leaching of arsenic in ground water is attributed to various factors, including excessive withdrawal of ground water for the purpose of irrigation, use of bio-control agents and phosphate fertilizers. It remains a mystery why all those who are exposed to arsenic-contaminated water do not develop the full-blown disease. Various host factors, such as nutritional status, socioeconomic status, and genetic polymorphism, are thought to make a person vulnerable to the disease. The approach to arsenicosis mitigation needs be holistic, sustainable, and multidisciplinary, with the 2 main pillars being health education and provision of 'arsenic-free water.' In the state of West Bengal, the drive for arsenic mitigation has been divided into 3 phases using various methods, including new hand pumps/tube wells at alternative deep aquifers, dug wells, arsenic removal plants, arsenic treatment units, as well as piped and surface water supply schemes. The methods have their own limitations, so it is intended that a pragmatic approach be followed in the arsenicosis prevention drive. It is also intended that the preventive measures be operationally and economically feasible for the people living in the affected areas.

Cryptic exposure to arsenic.

Arsenic is an odorless, colorless and tasteless element long linked with effects on the skin and viscera. Exposure to it may be cryptic. Although human intake can occur from four forms, elemental, inorganic (trivalent and pentavalent arsenic) and organic arsenic, the trivalent inorganic arsenicals constitute the major human hazard. Arsenic usually reaches the skin from occupational, therapeutic, or environmental exposure, although it still may be employed as a poison. Occupations involving new technologies are not exempt from arsenic exposure. Its acute and chronic effects are noteworthy. Treatment options exist for arsenic-induced pathology, but prevention of toxicity remains the main focus. Vitamin and mineral supplementation may play a role in the treatment of arsenic toxicity.