Toxicity of short‐term copper exposure to early life stages of red sea bream, Pagrus major

Abstract

Acute (0, 0.1, 0.2, 0.4, 0.8, 1.6 mg Cu/L) and chronic (0, 0.02, 0.04, 0.06, 0.08, 0.10, 0.12 mg Cu/L) toxicity tests of Cu with embryonic and larval red sea bream, Pagrus major, were carried out to investigate their biological responses to Cu exposure in static water at 18 +/- 1 degrees C (dissolved organic carbon, 1.8 +/- 0.65 mg C/L; hardness, 6,183 +/- 360 mg CaCO3/L; salinity, 33 +/- 1 per thousand). The 24- and 48-h LC50 (median lethal concentration) values of Cu for embryos were 0.23 and 0.15 mg/L, whereas the 48-, 72-, and 96-h LC50 values for larvae were 0.52, 0.19, and 0.13 mg/L, respectively, suggesting that embryos were more sensitive to Cu toxicity than larvae. Copper exposures at > or =0.06 mg concentrations caused low hatching success, a delay in the time to hatching of embryos, and reductions in the growth and yolk absorption of the larvae, whereas high mortality and morphological malformations occurred in the embryos and larvae at > or =0.08 mg/L concentrations. Copper concentration did not significantly affect the heart rate of the embryos, but it significantly decreased the heart rate of the newly hatched larvae when the Cu concentration was > or =0.08 mg/L, suggesting that Cu at high concentrations could induce heartbeat disturbances in red sea bream more easily at the larval stage than at the embryonic stage. Hatching success, time to hatching, growth rate, morphological abnormality, yolk absorption, and heart rate were Cu concentration-dependent and could be effective endpoints for evaluating Cu toxicity to the early life stages of red sea bream in nature.

Correlation between Congenital Heart Defects and maternal copper and zinc concentrations

“…Further investigations are needed to explore the potential sources of excessive copper concentrations. High copper concentrations are toxic to embryonic development, causing delayed development, malformations such as cardiac edema and declined heart rate (Cao et al, ). This suggests that excessive copper may cause negative effects to fetuses.…”

“…Copper ions serve as an important catalytic cofactor in the redox chemistry of proteins that carry out fundamental biological functions, such as: Cu/Zn SOD (Cu/Zn superoxide dismutase), cytochrome c oxidase, and ceruloplasmin (Shim and Harris, 2003). Copper deficiency induces heart teratogenesis in rats (Beckers-Trapp et al, 2006), and copper excess leads to an increase in the mortality of the embryos and larvae of Pagrus major (Cao et al, 2010). Zinc is an essential trace element for humans and is involved in the synthesis of many proteins, prokaryotic and eukaryotic nucleic acids and lipids (Falchuk and Montorzi, 2001).…”

Exposure to essential and non-essential trace elements and risks of congenital heart defects: A narrative review

“…Similarly, a specific pattern of cardiac malformation syndrome including double-outlet right ventricle, pulmonary hypoplasia and ventricular spetal defect has been detected in offspring of hamsters that exposed to excessive Cu during pregnancy ( 29 , 39 ). The abnormal morphological structures and impaired physiological functions of embryonic heart induced by Cu exposure have also been found in several model organisms such as red sea bream ( Pagrus major ) ( 40 ), rare minnow ( Gobiocypris rarus ) ( 28 ), and marine medaka ( Oryzias melastigma ) ( 41 ). Although the specific mechanisms are largely unknown, it has been proposed that impaired anti-oxidant system and altered development-related gene expression patterns may be responsible for Cu-induced cardiac malformation ( 28 ).…”

Maternal Zinc, Copper, and Selenium Intakes during Pregnancy and Congenital Heart Defects

“…Animal studies have shown that prenatal zinc deficiency during gestation led to heart malformations in offspring [ 5 ]. Copper deficiency induced heart anomalies in rats [ 6 ], and copper excess induced high mortality and morphological malformations in the embryos and larvae of Pagrus major [ 7 ]. Maternal selenium deficiency was reported to relate to miscarriages, premature births, and intrauterine growth retardation [ 8 , 9 , 10 ].…”