Introduction

The rise of energy drinks (EDs) since the 1980s has transformed consumer habits, with formulations designed for rapid energy boosts via stimulants and micronutrients [1]. Typical ED compositions include 80–300 mg/L caffeine, 1–4 g/L taurine, 0.2–2.4 g/L D-glucuronolactone, and B vitamins (e.g., B₃, B₆, B₁₂ at 100–300 % daily recommended intake), preserved with citric acid (pH 2.5–3.5) [1,2]. While marketed for performance enhancement, frequent ED consumption (up to 2–3 servings/day in 30 % of adolescents) correlates with oral health risks, including enamel erosion affecting 20–40 % of regular users [3,9].

Enamel erosion involves the chemical dissolution of hydroxyapatite [Ca₁₀(PO₄)₆(OH)₂] when oral pH falls below 5.5, the solubility threshold [4]. Acidic EDs drive this via protonation of enamel surfaces, but chelation—ligand-induced sequestration of Ca²⁺ into soluble complexes—amplifies demineralization by depleting lattice ions and inhibiting remineralization [10]. Citric acid exemplifies strong chelation (log K_Ca-citrate ≈ 3.5–4.8), yet the contributions of taurine, glucuronolactone, and B vitamins are emerging [2,5]. This review integrates biochemical, spectroscopic, and erosive assays to delineate their roles, drawing on studies by Lussi et al. [4] and Amaechi et al. [7], to inform dental preventive strategies.

Energetic drinks' erosivity stems from low pH (2.3–3.7), high titratable acidity (>15 mL 0.1 M NaOH/100 mL), and chelating additives that sustain ion dissolution [2]. In vitro models show EDs cause 0.39–1.01 mm³ enamel volume loss after 4-hour immersion, exceeding orange juice due to prolonged buffering [7]. Profilometric analysis reveals surface roughness (Ra) increases of 0.3–0.8 μm, while Vickers microhardness declines 25–45 % [3,11].

Taurine (β-aminoethanesulfonic acid), glucuronolactone (a glucuronic acid lactone), and B vitamins exceed nutritional needs in EDs (taurine: 1000–4000 mg/L; glucuronolactone: 600–2400 mg/L; B vitamins: 5–50 mg/L), potentially altering salivary Ca²⁺/PO₄³⁻ dynamics [1,6]. These components, while non-acidic, interact synergistically with citric acid to enhance Ca²⁺ mobility [5,10].

Molecular Mechanisms of Calcium Chelation:

1. Taurine and Calcium Binding

Taurine possesses a sulfonic acid group (-SO₃H, pKa ≈ 1.5–1.8) that deprotonates at ED pH, forming taurinate (Tau⁻) anions capable of monodentate Ca²⁺ coordination via electrostatic interactions [4]. Potentiometric studies estimate [Ca(Tau)]⁺ stability constants at log K ≈ 2.0–2.8, weaker than citrate but sufficient to form transient complexes that lower hydroxyapatite supersaturation by 10–15 % [4,10]. Lussi et al. [4] demonstrated taurine's role in prolonging low pH via Ca²⁺ scavenging, with in situ studies showing 15–20 % greater subsurface demineralization in taurine-enriched EDs (r=0.72, p<0.001). NMR spectroscopy confirms rapid (t_{1/2} < 2 min) binding to enamel surfaces, depleting pellicle Ca²⁺ and favoring erosion in athletes consuming 500 mL EDs daily [3,4].

2. Glucuronolactone (GlcA) and Calcium Interactions

Glucuronolactone hydrolyzes spontaneously in acidic media (rate constant k ≈ 0.05–0.15 min⁻¹ at pH 3) to D-glucuronic acid (GlcA), featuring a carboxyl group (-COOH, pKa 3.1–3.4) and vicinal hydroxyls for bidentate Ca²⁺ chelation [5]. The [Ca(GlcA)] complex has log K ≈ 3.8–4.2, comparable to mild EDTA derivatives, promoting Ca²⁺ extraction from hydroxyapatite lattices [5,13]. At ED pH <3.5, partial protonation limits binding, but deprotonated GlcA forms soluble Ca-GlcA salts (>40 mM solubility), competing with PO₄³⁻ for remineralization sites [5].

In vitro ICP-MS assays reveal 12–18 % enamel Ca²⁺ loss from glucuronolactone-supplemented EDs, with SEM showing etch pit depths of 8–12 μm after 10-min immersion [2,14]. Cavalcanti et al. [2] reported a 15–25 % increase in titratable acidity due to glucuronolactone's hydrolysis products, sustaining diffusion-limited erosion gradients. Related compounds like calcium-D-glucarate underscore this mechanism by sequestering Ca²⁺ and inhibiting β-glucuronidase, indirectly disrupting oral mineral homeostasis [13].

3. B Vitamins and Indirect Calcium Modulation

B vitamins act primarily as coenzymes but exert indirect chelating effects via functional groups. Pyridoxine (B₆) features an aldehyde moiety (log K_Ca ≈ 1.5–2.0) that forms pyridoxal-Ca²⁺ adducts, inhibiting Ca²⁺-dependent phosphatases and reducing salivary PO₄³⁻ by 10–20 % [6,15]. Elevated ED doses (20–100 mg/L) correlate with 8–12 % increased urinary Ca²⁺ excretion, per epidemiological data, via enhanced renal paracellular flux [15].

Cobalamin (B₁₂) coordinates Ca²⁺ through nitrogens (log K ≈ 2.0–2.5), perturbing ameloblast calmodulin signaling and enamel matrix mineralization [6]. Erosion models enriched with B vitamins show 10–15 % amplified Ca²⁺ dissolution, linked to upregulated acidogenic metabolism [6,16]. Higgins et al. [15] observed B₆ excess inducing enamel hypomineralization in rodents via Ca²⁺ disregulation. Let's summarize the data of our study in a table 1.

Table 1

Molecular Mechanisms of Calcium Chelation by Components of Energy Drinks

Discussion

Synergistic chelation by taurine, glucuronolactone, and B vitamins amplifies ED erosivity: taurine's weak binding sustains acidity [4], glucuronolactone boosts ion mobility [5], and B vitamins impair remineralization [6]. In vitro overestimates (e.g., static vs. dynamic flow) are tempered by clinical correlations (BEWE scores >9 in 25 % chronic users) [9]. Gaps include limited MD simulations for multi-ligand complexes and chronic in vivo data [10]. Calcium/phosphate fortification (e.g., 1–2 g/L CPP-ACP) counters effects, elevating pH by 0.4–0.8 and retaining 70–85 % hardness [8,17]. EFSA guidelines (taurine <4000 mg/day) warrant chelation-inclusive revisions [1].

Conclusion

Taurine, glucuronolactone, and B vitamins facilitate ED-mediated Ca²⁺ chelation via direct ligand binding and indirect metabolic modulation, intensifying enamel erosion [2,4,5,6]. Fortified formulations and usage limits hold therapeutic promise [8]. Prospective trials are crucial for mechanistic validation and public health policy. Further in vivo research is warranted to refine preventive guidelines.

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