Cleistanthus collinus induces type I distal renal tubular acidosis and type II respiratory failure in rats

Maneksh, Delinda; Sidharthan, Anita; Kettimuthu, Kavithapriya; Kanthakumar, Praghalathan; Lourthuraj, A. Amala; Ramachandran, Anup; Subramani, Sathya

doi:10.4103/0253-7613.66843

Cited by 11 publications

(7 citation statements)

References 17 publications

(13 reference statements)

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“…The terminal event in these test rats was respiratory arrest with bradycardia, and subsequent cardiac arrest. [ 56 ] The type 2 respiratory failure could be explained by the presence of neuromuscular blockade. This study did not demonstrate the occurrence of ECG abnormalities.…”

Section: Introductionmentioning

confidence: 99%

“…This study did not demonstrate the occurrence of ECG abnormalities. [ 56 ] Another study which examined the effect of the boiled extract on the rat heart had different observations. The study showed that low doses of extract caused transient tachycardia with increased myocardial contractility, while high doses caused arrhythmia and cardiac arrest.…”

Section: Introductionmentioning

confidence: 99%

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Cleistanthus collinus poisoning

Chrispal

2012

J Emerg Trauma Shock

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Cleistanthus collinus, a toxic shrub, is used for deliberate self-harm in rural South India. MEDLINE (PUBMED) and Google were searched for published papers using the search/ MeSH terms “Cleistanthus collinus,” “Euphorbiaceae,” “Diphyllin,” “Cleistanthin A,” Cleistanthin B” and “Oduvanthalai.” Non-indexed journals and abstracts were searched by tracing citations in published papers. The toxic principles in the leaf include arylnaphthalene lignan lactones — Diphyllin and its glycoside derivatives Cleistanthin A and B. Toxin effect in animal models demonstrate neuromuscular blockade with muscle weakness, distal renal tubular acidosis (dRTA) and type 2 respiratory failure with conflicting evidence of cardiac involvement. Studies suggest a likely inhibition of thiol/thiol enzymes by the lignan-lactones, depletion of glutathione and ATPases in tissues. V-type H+ ATPase inhibition in the renal tubule has been demonstrated. Mortality occurs in up to 40% of C. collinus poisonings. Human toxicity results in renal tubular dysfunction, commonly dRTA, with resultant hypokalemia and normal anion gap metabolic acidosis. Aggressive management of these metabolic derangements is crucial. Acute respiratory distress syndrome (ARDS) is seen in severe cases. Cardiac rhythm abnormalities have been demonstrated in a number of clinical studies, though the role of temporary cardiac pacemakers in reducing mortality is uncertain. Consumption of decoctions of C. collinus leaves, hypokalemia, renal failure, severe metabolic acidosis, ARDS and cardiac arrhythmias occur in severe poisonings and predict mortality. Further study is essential to delineate mechanisms of organ injury and interventions, including antidotes, which will reduce mortality.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cleistanthus collinus poisoning

Chrispal

2012

J Emerg Trauma Shock

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“…[ 18 ] The leaf extract of C. collinus produced type I distal renal tubular acidosis and type II respiratory failure in preclinical evaluations, and it was suggested that these changes are due to a decrease in the pH value of the urine, a failure of the acid-secreting mechanism and a decrease in the blood potassium levels. [ 16 ] In this study, no changes in urinary pH value (acidity) were observed with either cleistanthin A or cleistanthin B. As discussed earlier, one or more compounds other than cleistanthin A or cleistanthin B present in the leaf extract may be responsible for the acidosis and other effects on the kidneys.…”

Section: Discussionmentioning

confidence: 42%

“…The use of a C. collinus leaf extract is reported to have reduced the urinary pH value. [ 16 ] Since the leaves of C. collinus contain more than 30 compounds, it is possible that the reduction in pH was due to one or more compounds other than cleistanthins A and B. Although the compounds exert a diuretic activity as indicated by the diuretic index being greater than one, the extent of the effect is not comparable with that of furosemide.…”

Section: Discussionmentioning

confidence: 99%

Diuretic Effects of Cleistanthin A and Cleistanthin B from the Leaves of Cleistanthus Collinus in Wistar Rats

Parasuraman¹,

Raveendran²

2012

Journal of Young Pharmacists

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To study the diuretic effects of cleistanthin A and cleistanthin B, phytoconstituents were isolated from the leaves of Cleistanthus collinus in Wistar rats. The in vivo diuretic effects of cleistanthins A and B were determined according to the Lipschitz test. Prior to the experiment, the animals were fasted for 5 h and placed individually in metabolic cages. Cleistanthins A and B (12.5, 25, and 50 mg/kg) and furosemide (5 mg/kg) were suspended in 0.5% w/v carboxymethyl cellulose and administered orally. The urine was collected up to 5 h after administration and subsequently up to 24 h after administration. The acidity and urine volume were measured immediately. The urinary sodium and potassium levels were determined using a flame photometer, and the chloride level was determined by argentometric titration. The diuretic index and diuretic activity were calculated mathematically. While cleistanthins A and B showed a diuretic index of more than one, the diuretic activity of these compounds was less than one, indicating inferior activity compared with furosemide. Both cleistanthin A and B produced a significant increase in the urine volume and alterations in urinary electrolyte levels. However, the effect of the compounds was not dose dependent. Cleistanthin A and cleistanthin B exert diuretic effects in male Wistar rats without affecting the urinary acidity.

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“…that no evidence of cardiotoxicty was found in rats when the crude extract was given, and the present study also show similar results. [ 37 ]…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the antihypertensive activity and alpha adrenergic receptor interaction of cleistanthins A and B

Priyadharsini¹,

Parasuraman²,

Raveendran³

2014

J Basic Clin Pharma

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Hypertension was induced in male Sprague Dawley rats with twice weekly administration of deoxycorticosterone acetate (DOCA) salt (20 mg/kg s.c) for 4 weeks. They were divided into eight groups of six animals each viz., hypertensive control, standard (prazosin 1 mg/kg), cleistanthin A 12.5, 25, 50 mg/kg and cleistanthin B 12.5, 25 mg/kg, and 50 mg/kg. One more group served as normal control. The hypertension was induced in 4 weeks, and the animals were given assigned treatment in 5th week. The alteration in blood pressure (BP) was recorded weekly using a rodent noninvasive blood pressure system. At the end of the experiment alpha-adrenergic receptor response of drugs like adrenaline, nor adrenaline, dopamine (doses 1 μg and 2 μg) was recorded invasively. Two-way repeated measures ANOVA followed by Bonferroni post-hoc test was used to analyze the data. The systolic BP and diastolic BP of test groups rose to a higher level after DOCA administration and fell to the normal range (P < 0.05) following the administration of cleistanthins A and B. There were no differences in the weekly heart rate among the groups. In the test group animals pretreated with prazosin and cleistanthins, adrenaline, noradrenaline and dopamine failed to raise the mean arterial pressure and the end-diastolic pressure from baseline (P > 0.05) cleistanthins A and B exert a significant antihypertensive effect through alpha-adrenergic receptor blockade similar to prazosin.

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Cleistanthus collinus induces type I distal renal tubular acidosis and type II respiratory failure in rats

Cited by 11 publications

References 17 publications

Cleistanthus collinus poisoning

Cleistanthus collinus poisoning

Diuretic Effects of Cleistanthin A and Cleistanthin B from the Leaves of Cleistanthus Collinus in Wistar Rats

Evaluation of the antihypertensive activity and alpha adrenergic receptor interaction of cleistanthins A and B

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