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Purpose: This study investigates the anti-melanogenic effects of lotus seed and seedpod extract in B16F10 murine melanoma cells, and demonstrates the possible mechanisms involved in anti-pigmentation.Methods: The lotus seed and seedpod extracts were prepared using 70% ethanol as solvent. The irritation potential of the extracts was investigated using water-soluble tetrazolium salt (WST-1)-based cytotoxicity assay and expression analysis of the pro-inflammatory cytokine IL1β in B16F10 cells and HaCaT keratinocytes, respectively. The anti-melanogenic effects of the extracts were analyzed using intracellular melanin contents and tyrosinase activity assays. The effects of the extracts on tyrosinase expression were analyzed at the mRNA and protein levels. The effects of those extracts on the stability of tyrosinase protein were analyzed by evaluating the protein level after cycloheximide treatment.Results: WST-1-based cytotoxicity assay indicated that the concentration of ≤1.0% for lotus seed and seedpod extracts did not exhibit any cytotoxicity in B16F10 cells. Also, qRT-PCR analysis showed that the expression of IL-1β mRNAs was not increased by those concentrations of the extracts in HaCaT keratinocytes. Additionally, intracellular melanin contents assay showed that those extracts significantly inhibited α-MSH-induced melanin synthesis. Furthermore, cellular tyrosinase activity was significantly inhibited by the extracts. Additional investigations revealed that tyrosinase activity reduction was independent of its mRNA expression level, but dependent on its protein expression level. These findings were further confirmed by the results of the cycloheximide experiments stating that the protein stability of tyrosinase was reduced after the treatment with those extracts.Conclusion: Lotus seed and seedpod extracts showed anti-pigmentation effects by accelerating degradation of tyrosinase protein at the post-translation level in B16F10 cells.

The toxicokinetic profiles of phthalic acid (PA), which is the common final metabolite of phthalic acid esters (PAE), were studied in rats after orally administering doses 20, 100, or 500 mg/kg. Concentrations of PA were determined in serum or urine by high-performance liquid chromatography (HPLC). The plasma concentrations of PA showed a biexponential increase following oral administration of doses ranging from 20 to 500 mg/kg. The terminal elimination half-lives (t1/2) of PA at dosages of 20, 100, or 500 mg/kg were 6.46 +/- 1.13, 5.19 +/- 3.56, and 5.10 +/- 1.10 h, respectively, total clearances (Cl/F) of PA at 20, 100, or 500 mg/kg were 97.43 +/- 4.20, 215.01 +/- 55.42, and 721.07 +/- 51.81 ml/h, and apparent distribution volumes of PA in the steady state (Vz/F) at 20, 100, or 500 mg/kg were 903.28 +/- 125.28, 1419.87 +/- 527.53, and 5264.86 +/- 993.65 ml, respectively. PA was absorbed rapidly after an oral dose of 500 mg/kg with peak concentration (Cmax) in blood (3.5 +/- 0.33 microg/ml) at 30 min postadministration. After oral administration, the dose-normalized area under the curve (AUC) (146.90 +/- 9.33 microg/h/ml) for 500 mg/kg was significantly greater than at 20 mg/kg (44.69 +/- 2.56 microg/h/ml). Urine analysis indicated that 13 +/- 0.45% of the administered PA dose (at 500 mg/kg, p.o.) was recovered unchanged in urine within 24 h. Data concerning the toxicokinetic profiles of PA improve our understanding of the toxicological potential of PAE and may prove useful for risk assessments of multiple phthalates exposure.

A mathematical model was developed to describe the motion resistance of rigid wheels under self-propelled conditions where no drawbar pull is developed. The modeling was based on the concept that the work required to overcome the motion resistance is equal to the energy dissipated in compacting the soil beneath the wheel. Slippage of the wheel was also considered in the modeling. Finally the validity of the proposed model was discussed.