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Tungsten, due to its distinguished physical properties, has wide industrial and military applications. Environmental exposure to tungsten, which mainly occurs through various sources like food, water, soil, etc., is of growing concern as various toxic effects have recently been reported. In this study, we investigated the effects of oral and intraperitoneal (i.p.) administration of sodium tungstate on various biochemical variables indicative of oxidative stress in erythrocytes and soft tissue damage in rats. Male rats were administered to 119 mg, 238 mg/kg of sodium tungstate orally or 20 mg and 41 mg/kg through i.p. route, for 14 consecutive days. The results demonstrated a significant increase in Reactive Oxygen Species (ROS) and an increase in catalase and glutathione peroxidase antioxidant enzymes activities in erythrocytes. Erythrocyte glutathione-S-transferase (GST) activity showed significant inhibition, while tissue ROS and thiobarbituric acid reactive substance levels increased accompanied by a decreased reduced glutathione, oxidized glutathione (GSH:GSSG) ratio. These changes were supported by an increase in plasma transaminases activities, creatinine, and urea levels, suggesting hepatic and renal injury. These biochemical alterations were prominent in rats intraperitoneally administrated with sodium tungstate than oral administration, suggesting more pronounced toxicity. The study also suggests oxidative stress as one of the major mechanism involved in the toxic manifestations of sodium tungstate.

In the coming decades, eliminating malaria is the foremost goal of many tropical countries. Transmission control, along with an accurate and timely diagnosis of malaria, effective treatment and prevention are the different aspects that need to be met synchronously to accomplish the goal. The current review is focused on one of these aspects i.e., transmission control, by looking deeper into the event called gametogenesis. In the Plasmodium life cycle, gametocytes are the first life forms of the sexual phase. The transmission of the parasite and the disease is critically dependent on the number, viability and sex ratio of mature gametocytes and their further development inside mosquito vectors. Gametogenesis, the process of conversion of gametocytes into viable gametes, takes place inside the mosquito midgut, and is a tightly regulated event with fast and multiple rounds of DNA replication and diverse cellular changes going on within a short period. Interrupting the gametocyte-gamete transition is ought to restrict the successful transmission and progression of the disease and hence an area worth exploring for designing transmission-blocking strategies. This review summarizes an in-depth and up-to-date understanding of the biochemical and physiological mechanism of gametogenesis in Plasmodium, which could be targeted to control parasite and malaria transmission. This review also raises certain key questions regarding gametogenesis biology in Plasmodium and brings out gaps that still accompany in understanding the spectacular process of gametogenesis.

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Tungsten has no known function in humans and is a relatively new contaminant, whereas molybdenum, its congener in the periodic table, is a nutritionally essential element. In addition to early studies on molybdosis in ruminants, their toxic effects in the form of tungstate and molybdate have been addressed primarily in rodents and are predominantly mediated by inducing oxidative stress in various tissues. The purpose of this study was to evaluate the differences between tungstate and molybdate in human liver (HepG2) and kidney (HEK293) cell lines in terms of retention in cells, effect on reactive oxygen species, and activities of xanthine oxidase and phosphatases. The cell lines were exposed to tungstate or molybdate (1 mM to 10 mM) for 24 h, lysed and analyzed for the above biochemical parameters. Despite the chemical similarity of the two anions, cell-specific differential effects were observed. At all concentrations, tungstate was retained more in HEK293 cells while molybdate was retained more in HepG2 cells. HepG2 cells were more sensitive to tungstate than molybdate, showing reduced viability at concentrations as low as 10 mM. Exposure to either anion resulted in the inhibition of protein tyrosine phosphatases at 1 mM and an increased production of reactive oxygen species (ROS) at 100 mM despite their inhibition of the ROS-producing molybdenum enzyme xanthine oxidase. In conclusion, the results indicate that excess of nutritionally essential molybdate or non-essential tungstate causes toxicity by affecting ROS-and phosphorylation-dependent signaling pathways and ensuing gene expression.