Impact of bicarbonate, ammonium chloride, and acetazolamide on hepatic and renal SLC26A4 expression

SLC26A4 encodes pendrin, a transporter exchanging anions such as chloride, bicarbonate, and iodide. Loss of function mutations of SLC26A4 cause Pendred syndrome characterized by hearing loss and enlarged vestibular aqueducts as well as variable hypothyroidism and goiter. In the kidney, pendrin is expressed in the distal nephron and accomplishes HCO(3)(-) secretion and Cl(-) reabsorption. Renal pendrin expression is regulated by acid-base balance. The liver contributes to acid-base regulation by producing or consuming glutamine, which is utilized by the kidney for generation and excretion of NH(4)(+), paralleled by HCO(3)(-) formation. Little is known about the regulation of pendrin in liver. The present study thus examined the expression of Slc26a4 in liver and kidney of mice drinking tap water without or with NaHCO(3) (150 mM), NH(4)Cl (280 mM) or acetazolamide (3.6 mM) for seven days. As compared to Gapdh transcript levels, Slc26a4 transcript levels were moderately lower in liver than in renal tissue. Slc26a4 transcript levels were not significantly affected by NaHCO(3) in liver, but significantly increased by NaHCO(3) in kidney. Pendrin protein expression was significantly enhanced in kidney and reduced in liver by NaHCO(3). Slc26a4 transcript levels were significantly increased by NH(4)Cl and acetazolamide in liver, and significantly decreased by NH(4)Cl and by acetazolamide in kidney. NH(4)Cl and acetazolamide reduced pendrin protein expression significantly in kidney, but did not significantly modify pendrin protein expression in liver. The observations point to expression of pendrin in the liver and to opposite effects of acidosis on pendrin transcription in liver and kidney

Edible Ectomycorrhizal Mushroom Molecular Response to Heavy Metals

Heavy metal pollution poses a significant threat to the environment, public, and soil health. Ectomycorrhizal fungi are thought to enhance mineral nutrition of their host plants and to confer increased tolerance toward toxic metals. The responses of mycorrhizal fungi to toxic metal cations are diverse and may consist of a reduced uptake of metals by extracellular or intracellular chelation or increased efflux out of the cell or into sequestering compartments. Rhizosphere chemistry is critical to understanding the interactions of mycorrhizae with polluted soils. This, linked to the fact that mycorrhizal diversity is normally high, even on highly contaminated sites, suggests that this diversity may have a significant role in colonization of contaminated sites by ectomycorrhizal fungi. However, the molecular mechanisms underlying the response of ectomycorrhizal fungi to heavy metals in general remain poorly understood, although the recent Tuber melanosporum Vittad. genome sequencing and transcriptome analyses have obtained a global view of metal homeostasis-related genes and pathways in this fungus. The focus of this review is to describe and discuss the tolerance of the ectomycorrhizal fungi, in particular the edible ones, under heavy metal stress conditions