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the reducing agent

Acute Exposure/ The ingestion of ammonium chloride in doses of around 500-1000 mg/kg bw/day, for periods ranging from 1 to 8 days, has induced metabolic acidosis in mice, guinea-pigs, rats, rabbits, and dogs. However, /one study/ did not report any toxic effects at doses of up to 1 g/kg bw in rats, rabbits, guinea-pigs, and cats (50 animals per group). Clinical signs, depending on the severity of the acidosis, include: a decrease in plasma- and urinary-pH; decreased appetite; decreased carbon dioxide-combining power; an increase in BUN and chlorides; an increase in plasma proteins; an increase in hematocrit (hemoconcentration); increased gluconeogenesis; increased phosphoenolpyruvate carboxykinase activity; increased urinary ammonium; increased urea, sodium, chloride, calcium, and titratable acid excretion; an increase in malate and oxaloacetate concentrations in renal tissue; and decreased concentrations of glutamine, glutamate, and alpha-ketoglutarate in the kidney. Pulmonary edema, central nervous system dysfunction, and renal changes are reported to have occurred after ingestion of ammonium chloride. Susceptibility to ammonium chloride differs among species. For instance, pulmonary edema is produced in cats, but not in rabbits; yet cats have been shown to be more resistant to oral poisoning by ammonium chloride than other animals studied.