The Water-Soluble Fraction (&lt;10 kD) of Bee Venom &lt;i&gt;(Apis mellifera)&lt;/i&gt; Produces Inhibitory Effect on Apical Transporters in Renal Proximal Tubule Cells

Han, Ho Jae; Yoon, Byeong Cheol; Oh, Young J.; Park, Soo Hyun; Lee, Jang Hern; Mar, Woongchon

doi:10.1159/000068696

Cited by 7 publications

(7 citation statements)

References 30 publications

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“…9 Melittin also inhibits the uptake of sodium, phosphate and α-methyl-d-glucopyranoside in proximal renal tubules, but it increases proximal tubule calcium uptake with resultant arachidonic acid release. 63 These effects are believed to presage renal tubular injury. Calcium uptake is inhibited by mepacrine, verapamil and nifedipine.…”

Section: Pathophysiologymentioning

confidence: 99%

Animal toxins and the kidney

Sitprija

2008

Nat Rev Nephrol

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Envenomation or poisoning by toxins from animals poses an important health hazard in the tropics. Animal toxins are complex mixtures of proteins, peptides, enzymes and chemicals. These toxins exert their effects through modulation of ion channels and receptors, and via direct enzyme action. Depolarization or hyperpolarization of ion channels--caused by most marine toxins, and some snake and insect venoms--results in neuromuscular symptoms that can be associated with hemodynamic changes. Toxin enzymes, especially proteases and phospholipase A2, initiate inflammatory processes that involve the generation of proinflammatory cytokines and vasoactive mediators, resulting in systemic and renal hemodynamic alterations. Toxin enzymes also have direct effects on erythrocytes, myocytes, blood coagulation factors, vascular endothelium and epithelial cells. As a result, disseminated intravascular coagulation, bleeding diathesis, intravascular hemolysis and rhabdomyolysis are common after exposure to animal toxins. The renal manifestations of animal toxin envenomation, which are usually acute, result mainly from these enzymatic effects. All renal structures can be affected by animal toxins, and tubular necrosis is common. Acute kidney injury is attributed to decreased renal blood flow (associated with intravascular hemolysis or rhabdomyolysis), disseminated intravascular coagulation or direct tubular toxicity. Immunologic mechanisms have a minor role in the pathophysiology of nephropathy caused by animal toxins.

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Section: Pathophysiologymentioning

confidence: 99%

Animal toxins and the kidney

Sitprija

2008

Nat Rev Nephrol

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“…channels expressed mainly in the central nervous system and also in intestinal myocytes, hepatocytes, and endothelial cells [4]. There is also evidence of significant increases in fractional excretion of sodium and potassium in animals injected with Africanized bee venom [5]. Other studies showed that mellitin, another component of bee venom, inhibits apical transporters of proximal tubules [6].…”

Section: Discussionmentioning

confidence: 99%

Fanconi syndrome following honeybee stings

et al. 2010

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A 32-year-old gentleman was attacked by honey bees about 8 months and immediately afterwards his eyelids, cheeks and pinnae became swollen, red, and tender. However, the patient did not develop any renal or serum sickness symptoms and his physical examination and laboratory investigations were normal. He recovered completely. A week later, while working on his farm, he experienced a sudden loss of muscular tone in all four limbs without losing his consciousness. The medical examination subsequently revealed flaccid quadriparesis associated with a serum potassium of 2.1 mEq/L. He was also found to have hyperchloremic metabolic acidosis with normal anion gap and preserved ability to acidify urine to a pH of 5.5. These findings were suggestive of proximal renal tubular acidosis (Fanconi syndrome). Other abnormalities like hypophosphataemia, hypouricemia, renal glucosuria and high urinary excretion of calcium, phosphorus and uric acid further supported the diagnosis of proximal tubular dysfunction. The renal biopsy revealed dense lymphocytic interstitial infiltrate, a feature often seen in Sjogren's syndrome, in which at least 50% of patients fail to acidify urine. In our patient, thorough search for other causes of proximal renal tubular acidosis was negative.

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“…Melittin is a peptide in bee ( Apis mellifera ) venom. Melittin inhibits proximal tubular reabsorption of α methyl D‐glucopyranoside, aminoacid and phosphate . Inhibition of α methyl D‐glucopyranoside by melittin is through lipid peroxidation and increased arachidonic acid and is prevented by mepacrine and AACOCF3, PLA2 inhibitors .…”

Section: Bee Venommentioning

confidence: 99%

“…Regulation of SGLT expression and localization is cAMP and PKA dependent through caveolin‐1 and F‐actin activation . Experimentally, melittin decreases luminal transport of α methyl D‐glucopyranoside, aminoacid and phosphate, indicating inhibition of cotransport in proximal tubules . α methyl D‐glucopyrenoside is used a selective tracer of Na dependent glucose transport.…”

Section: Scorpion Envenoming and Renal K Transportmentioning

confidence: 99%

“…Melittin inhibits proximal tubular reabsorption of α methyl D-glucopyranoside, aminoacid and phosphate. 25 Inhibition of α methyl D-glucopyranoside by melittin is through lipid peroxidation and increased arachidonic acid and is prevented by mepacrine and AACOCF3, PLA2 inhibitors. 26 Melittin is a strong PLA2 stimulator and inhibits NHE3 either directly or through Na K-ATPase inhibition or through 20-HETE.…”

Section: Bee Venom Melittinmentioning

confidence: 99%

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Animal toxins and renal ion transport: Another dimension in tropical nephrology

Sitprija

2016

Nephrology

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Sitprija et al have reviewed the issue regarding renal vascular and renal tubular ion channels and transporters involved in animal toxin injury. Several vascular and renal tubular ion channels have been modulated by various animal toxins, resulting in hemodynamic alterations. ABSTRACT:Renal vascular and tubular ion channels and transporters involved in toxin injury are reviewed. Vascular ion channels modulated by animal toxins, which result in haemodynamic alterations and changes in blood pressure, include ENaC/Degenerin/ASIC, ATP sensitive K channels (KATP), Ca activated K channels (Kca) and voltage gated Ca channels, mostly L-type. Renal tubular Na channels and K channels are also targeted by animal toxins. NHE3 and ENaC are two important targets. NCC and NKCC may be involved indirectly by vasoactive mediators induced by inflammation. Most renal tubular K channels including voltage gated K channels (Kv1), KATP, ROMK1, BK and SK are blocked by scorpion toxins. Few are inhibited by bee, wasp and spider venoms. Due to small envenoming, incomplete block and several compensatory mechanisms in renal tubules, serum electrolyte charges are not apparent. Changes in serum electrolytes are observed in injury by large amount of venom when several channels or transporters are targeted. Envenomings by scorpions and bees are examples of toxins targeting multiple ion channels and transporters.

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The Water-Soluble Fraction (<10 kD) of Bee Venom <i>(Apis mellifera)</i> Produces Inhibitory Effect on Apical Transporters in Renal Proximal Tubule Cells

Cited by 7 publications

References 30 publications

Animal toxins and the kidney

Animal toxins and the kidney

Fanconi syndrome following honeybee stings

Animal toxins and renal ion transport: Another dimension in tropical nephrology

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