Short-term alteration of nitrogen supply prior to harvest affects quality in hydroponic-cultivated spinach (Spinacia oleracea).

BACKGROUND: Quality-associated problems, such as excessive in planta accumulation of oxalate, often arise in soillessly cultivated spinach (Spinacia oleracea). Maintaining a higher level of ammonium (NH4⁺) compared to nitrate (NO3⁻) during the growth period can effectively decrease the oxalate content in hydroponically cultivated vegetables. However, long-term exposure to high concentrations of NH4⁺ induces toxicity in plants, and thus decreases the biomass production. Short-term application of NH4⁺ before harvesting in soilless cultivation may provide an alternative strategy to decrease oxalate accumulation in spinach, and minimise the yield reduction caused by NH4⁺ toxicity. RESULT: The plants were pre-cultured in 8 mmol L⁻¹ NO3⁻ nutrient solution. Next, 6 days before harvest, the plants were transferred to a nutrient solution containing 4 mmol L⁻¹ NO3⁻ and 4 mmol L⁻¹ NH4⁺. This new mix clearly reduced oxalate accumulation, increased levels of several antioxidant compounds, and enhanced antioxidant capacity in the edible parts of spinach plants, but it did not affect biomass production. However, when the 8 mmol L⁻¹ NO3⁻ was shifted to either nitrogen-free, 4 mmol L⁻¹ NH4⁺ or 8 mmol L⁻¹ NH4⁺ treatments, although some of the quality indexes were improved, yields were significantly reduced. CONCLUSIONS: Short-term alteration of nitrogen supply prior to harvest significantly affects quality and biomass of spinach plants, and we strongly recommend to simultaneously use NO3⁻ and NH4⁺ in hydroponic cultivation, which improves vegetable quality without decreasing biomass production.

Lanthanum carbonate inhibits intestinal oxalate absorption and prevents nephrocalcinosis after oxalate loading in rats.

PURPOSE: Increased intestinal oxalate absorption leads to increased urinary oxalate excretion (secondary hyperoxaluria) and calcium oxalate crystal formation, contributing to nephrocalcinosis/lithiasis. Lanthanum carbonate is an intestinal phosphate binder that is orally administered to patients on dialysis to treat hyperphosphatemia. It is hypothesized that lanthanum can also bind oxalate, in addition to phosphate. We evaluated this in vitro and in vivo. MATERIALS AND METHODS: In vitro oxalate binding was evaluated by oxalate precipitation from a solution by lanthanum. In vivo oxalate absorption kinetics and the effect of lanthanum carbonate on nephrocalcinosis development were assessed in male Sprague-Dawley® rats that received 1) 1,000 mg lanthanum carbonate and oxalate, 2) carboxymethylcellulose and oxalate or 3) carboxymethylcellulose by gavage for up to 12 hours (kinetics) or 7 days (nephrocalcinosis). Plasma and urinary oxalate concentrations were measured at several time points after gavage. The degree of nephrocalcinosis was assessed histomorphometrically on von Kossa stained sections and by measuring total calcium content in renal tissue. RESULTS: In vitro lanthanum bound oxalate in a pH range comparable to the range of the intestine. In vivo oxalate administration in untreated animals resulted in a biphasic pattern of increased plasma oxalate levels, which was almost abolished in lanthanum treated rats. In the urine of treated rats oxaluria and calcium oxalate crystalluria were blunted. Moreover, significantly decreased nephrocalcinosis was observed compared with that in untreated rats. CONCLUSIONS: Lanthanum carbonate is a promising agent for the future prevention/treatment of secondary hyperoxaluria.

Cadmium-induced oxalate secretion from root apex is associated with cadmium exclusion and resistance in Lycopersicon esulentum.

The mechanisms of heavy metal resistance in plants can be classified into internal tolerance and exclusion mechanisms, but exclusion of heavy metals with the help of organic acids secretion has not been well documented. Here we demonstrated the contribution of oxalate secretion to cadmium (Cd) exclusion and resistance in tomato. Different Cd resistance between two tomato cultivars was evaluated by relative root elongation (RRE) and Cd accumulation. Cultivar 'Micro-Tom' showed better growth and lower Cd content in roots than 'Hezuo903' at different Cd concentrations not only in short-term hydroponic experiment but also in long-term hydroponic and soil experiments, indicating that the genotypic difference in Cd resistance is related to the exclusion of Cd from roots. 'Micro-Tom' had greater ability to secrete oxalate, suggesting that oxalate secretion might contribute to Cd resistance. Cd-induced secretion of oxalate was localized to root apex at which the majority of Cd accumulated. Phenylglyoxal, an anion-channel inhibitor, effectively blocked Cd-induced oxalate secretion and aggravated Cd toxicity while exogenous oxalate supply ameliorated Cd toxicity efficiently. These results indicated that the oxalate secreted from the root apex helps to exclude Cd from entering tomato roots, thus contributes to Cd resistance in the Cd-resistant tomato cultivar.

Effect of verapamil on urinary stone-forming risk factors.

Prevention of recurrent stone formation will only be possible with careful metabolic evaluation and appropriate management. In this present prospective study, a total of 95 patients with calcium oxalate (CaOx) stone disease were evaluated with respect to the effects of a calcium channel blocking agent (verapamil) therapy on stone-forming risk factors. A total of 95 patients with CaOx urolithiasis were well evaluated for the possible specific effects of verapamil administration on stone-forming risk factors during long-term follow-up. All patients had calcium-containing stones with normal renal morphology and function without any urinary tract infection. The follow-up period ranged from 12 to 36.6 months, with a mean value of 24.4 months. The age of the patients (54 male and 41 female; M/F: 1.31) ranged from 20 to 46 years (mean 34.3 years). On metabolic evaluation all patients had some kind of risk factors and patients were independently randomized into two groups, namely group 1 (n = 49): patients receiving calcium entry blocker, verapamil hydrochloride (isoptin 240 mg KKH tablets, oral t.i.d.); group 2 (n = 46): patients receiving no specific therapy (control patients) that were matched for sex and age. Follow-up results (at least 1 year) with respect to the changes in urinary stone-forming risk factors were recorded in both groups. During long-term follow-up patients undergoing no specific therapy did not show a significant change with respect to the urinary levels of stone-forming risk factors when compared with the others receiving verapamil on a regular basis. In the light of our results as well as the literature data, we believe that the pathophysiological mechanisms underlying the effect of verapamil on stone formation (as a result of enhanced crystal deposition) and on the excretion of the urinary stone-forming risk factors have to be well evaluated in further experimental as well as clinical studies. Although the exact mechanism of action is not clear; we may claim that the limitation of internal calcium shift by these agents may also well effect the tubular process related to oxalate handling which ultimately limits its excretion in urine.

Studies on some possible biochemical treatments of primary hyperoxaluria.

The effects of some putative inhibitors of oxalate production or urinary oxalate excretion have been investigated in the Cynamolgus monkey and in patients with Type I primary hyperoxaluria (hyperoxaluria with glycollic aciduria). Sodium-1-hydroxybutan-sulphonate, D,L-phenyllactate, succinimide and isocarboxazide did not reduce the urinary oxalate excretion in the monkeys. Pyridoxine reduced the excretion of oxalate and glycollate in some patients, and its therapeutic use has been documented over a five-year period. Succinimide, which has been used by other workers for the treatment of non-hyperoxaluric stone formers, did not decrease the excretion of either oxalate or glycollate in three patients in whom it was tried. It did not change the inhibitory activity of the urine with respect to the growth and aggregation of calcium oxalate crystals in any of the three patients, and it did not have any consistent effect on the excretion of calcium oxalate crystals in the one patient who had detectable crystaluria before treatment. We have identified several metabolites of succinimide in the urine of patients taking the drug. These include 2,3-dehydrosuccinamic, 2-hydroxysuccinamic and 3-hydroxysuccinamic acids. Isocarboxazide, cholestyramine and thiamine did not affect the urinary oxalate excretion in the patients. The significance of these observations from the viewpoint of the treatment of primary hyperoxaluria is discussed.

Inhibitors and promoters of stone formation.

The understanding of the formation of urinary stones centers around three main mechanisms: the urinary concentration of stone-forming ions, the role of promoters, and the role of inhibitors of crystal formation and crystal aggregation. With respect to the promoting activity, lately emphasis has shifted from the role of the organic matrix to that of one salt inducing by epitaxy the precipitation of another salt. Among the inhibitors, it has become necessary to distinguish between those affecting crystal formation and those affecting crystal aggregation. For measuring the inhibitory activity, the various techniques and their relevance have been reviewed. It has been found that the main inhibitors for calcium phosphate and calcium oxalate precipitation are citrate, pyrophosphate, and perhaps magnesium. Those for calcium phosphate and calcium oxalate aggregation are glycosaminoglycans, pyrophosphate, and citrate. Among the synthetic inhibitors, the diphosphonates are the most powerful for both processes. The role and the therapeutic implications of these various concepts have been discussed.

Methylene blue as an inhibitor of stone formation.

Kinetics of growth and dissolution of calcium oxalate monohydrate were examined in the presence of small concentrations of methylene blue. The data presented show moderate retardation in growth and dissolution rates. It was also found that methylene blue decreased the decalcification rate of calcium oxalate renal calculi. The implications of these findings in the treatment of urolithiasis are discussed.

Growth of calcium oxalate crystals. II. Inhibition by natural urinary crystal growth inhibitors.

A method is described for quantitatively determining the inhibitory activity of pure components, isolates, or mixtures of components (such as urine) on the growth of calcium oxalate crystals. Results with known calcium phosphate crystal growth inhibitors--magnesium, citrate, and pyrophosphate--suggest that these components contribute little to the ability to normal urine to inhibit the growth of calcium oxalate crystals. As yet unidentified urinary components seem to be responsible for most of this activity. The urinary crystal growth inhibitors appear to function by adsorbing on the surface of the growing crystals, thereby preventing the further incorporation of lattice ions. The fit of experimental data to the Langmuir absorption isotherm supports this conclusion.

Effect of diphosphonate on crystallization of calcium oxalate in vitro.

Reliable techniques for the calculation of activity product (state of saturation), formation product (limit of metastability) and crystal growth of calcium oxalate were devised. The activity product at saturation was 2.53 times 10 minus 9 M2, and was independent of duration of incubation, solid-to-solution ratio, pH, calcium concentration or ionic strength. These tehcniques were utilized to assess the effect of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP) on crystallization of calcium oxalate in an aqueous salt solution in vitro. EHDP increased the formation product of calcium oxalate, indicating an inhibition of nucleation of calcium oxalate. Further, it inhibited the crystal growth of calcium oxalate.