Long-Term Exposure of the Red Cherry Shrimp Neocaridina davidi to Diclofenac: Impact on Survival, Growth, and Reproductive Potential

What was studied

Study shape: Twenty-two aquaria were randomly assigned per treatment. Each began with one ovigerous female and two mature males and received control water or nominal 0.1 or 1 mg/L diclofenac. HPLC-MS/MS checks at 0 and 72 hours in two aquaria per treatment produced overall measured means of 0.0075, 0.1320 and 1.0730 mg/L, respectively. Mortality, molts, egg loss, hatching and ovarian rematuration were checked daily; surviving adults, broods, ovaries and male distal vas deferens supplied later endpoints.

Experimental unit: The 1.5-litre aquarium, with 22 aquaria per assigned treatment

Endpoints: mortality, adult specific growth rate, successive spawning timing, hatching, juvenile count and morphology, female ovarian histology, male spermatophore histology.

Claim boundary

What it can support: Under this 63-day laboratory protocol, aggregate mortality was 22.7, 39.4 and 45.5 percent, with only the 1 mg/L nominal treatment differing significantly from control. The higher treatment reduced survivor-conditioned female growth, the proportion of females hatching their first exposed brood and the proportion of advanced ovarian oocytes, shortened interspawn timing, and increased abnormal juveniles per female in the small second-spawn sample. Incubation time, male growth, male spermatophore structure and among-treatment hatchling counts did not differ significantly.

What it cannot support: The control was not an analytical zero: its two checks were 0.009 and 0.006 mg/L, for a 0.0075 mg/L mean. The lowest nonzero measured treatment averaged 0.1320 mg/L, and only two nonzero treatments were tested. Analytical checks covered two aquaria per treatment at two times. The first egg cohort had already developed partly before exposure, later brood and tissue endpoints were conditioned on female survival and successful spawning, the second-spawn abnormality result came from few females, and male dependency may not have been fully represented by aquarium in the analysis. Stock came from a dealer-derived laboratory colony without voucher or diagnostic identity confirmation; allocation blinding, feed intake, exposure-period nitrogen chemistry, tissue residues and offspring survival or growth were not reported. The preprint abstract can overstate the juvenile-count result because the paper reports no significant among-treatment decrease. The design does not establish a trace-effect threshold, safe household medication concentration, aquarium treatment, recovery, mechanism or multigeneration outcome. The SSRN and Research Square postings are duplicate preprint versions, not independent replication.

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