English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background   Previous studies on cryptolepine, the antimalarial and cytotoxic alkaloid of  Cryptolepis sanguinolenta , showed that it preferentially accumulates in rapidly proliferating cells and melanin-containing tissues. Subsequently, we demonstrated that cryptolepine was toxic to murine embryos  in vivo  but no signs of teratogenicity.  in vivo  developmental studies can be confounded by maternal effects. Here, we hypothesized that cryptolepine-induced embryo toxicity occurs at least partly through direct inhibition of embryogenesis rather than indirectly through the induction of maternal toxicity.Aim   To determine the effects of cryptolepine on developing zebrafish embryos  ex vivo .Methods   Healthy synchronized zebrafish eggs were treated with cryptolepine (10 −1  − 5 × 10 2   μ M), benzyl penicillin (6 − 6 × 10 2   μ M), or mercury chloride (3.7 × 10 −1  − 3.7 × 10 1  nM) from 6 to 72 hours postfertilization. Developing embryos were assessed at 24, 48, 72, and 96 hours under microscope for lethality, hatching rate, and malformation.Results   LC 50  for cryptolepine in the study was found to be 260 ± 0.174  μ M. Cryptolepine induced dose- and time-dependent mortality from the 24 to 96 hours postfertilization. Lower cryptolepine concentration (<100  μ M) caused mortality, approximately 15–18%, only after the 48 hours postfertilization. The most sensitive period of embryo lethality corresponded well with the pharyngula (24 to 48 hours) and hatching (48 to 72 hours) stages of embryonic development. Cryptolepine (10 −1  − 5 × 10 2   μ M) dose dependently inhibited the hatching rate. At doses above 500  μ M, hatching was completely inhibited. Mercury chloride (3.7 × 10 −1  − 3.7 × 10 1  nM), used as positive control, induced a consistent pattern of embryo lethality at all stages of development, whereas benzyl penicillin (6 − 6 × 10 2   μ M), used as negative control, did not induce any significant embryo lethality. Morphological examination of (postfertilization day 5) of eleutheroembryos treated during embryonic development with cryptolepine showed decreased body length (growth inhibition), decreased eye diameter and bulginess, enlarged pericardia, and enlarged yolk sac and muscle malformations.Conclusion   Cryptolepine induces malformations, growth retardation, and mortalities in rapidly dividing zebrafish embryos  ex vivo .

Cryptolepine, the Main Alkaloid of the Antimalarial Cryptolepis sanguinolenta (Lindl.) Schlechter, Induces Malformations in Zebrafish Embryos