Polycyclic aromatic hydrocarbons (PAHs) are organic compounds that are widely distributed in the air, water, and soil. Recently, the amount of PAHs derived from fuels and from incomplete combustion processes is increasing. In the aquatic environment, oil spills directly cause PAH pollution and affect marine organisms. Oil spills correlate very well with the major shipping routes. Furthermore, accidental oil spills can seriously impact the marine environment toxicologically. Here, we describe PAH toxicities and related bioaccumulation properties in aquatic animals, including invertebrates. Recent studies have revealed the toxicity of PAHs, including endocrine disruption and tissue-specific toxicity, although researchers have mainly focused on the carcinogenic toxicity of PAHs. We summarize the toxicity of PAHs regarding these aspects. Additionally, the bioaccumulation properties of PAHs for organisms, including invertebrates, are important factors when considering PAH toxicity. In this review, we describe the bioaccumulation properties of PAHs in aquatic animals. Recently, microplastics have been the most concerning environmental problem in the aquatic ecosystem, and the vector effect of microplastics for lipophilic compounds is an emerging environmental issue. Here, we describe the correlation between PAHs and microplastics. Thus, we concluded that PAHs have a toxicity for aquatic animals, indicating that we should emphasize the prevention of aquatic PAH pollution.

Astronauts experience osteoporosis‐like loss of bone mass because of microgravity conditions during space flight. To prevent bone loss, they need a riskless and antiresorptive drug. Melatonin is reported to suppress osteoclast function. However, no studies have examined the effects of melatonin on bone metabolism under microgravity conditions. We used goldfish scales as a bone model of coexisting osteoclasts and osteoblasts and demonstrated that mRNA expression level of acetylserotonin O‐methyltransferase, an enzyme essential for melatonin synthesis, decreased significantly under microgravity. During space flight, microgravity stimulated osteoclastic activity and significantly increased gene expression for osteoclast differentiation and activation. Melatonin treatment significantly stimulated Calcitonin (an osteoclast‐inhibiting hormone) mRNA expression and decreased the mRNA expression of receptor activator of nuclear factor κB ligand (a promoter of osteoclastogenesis), which coincided with suppressed gene expression levels for osteoclast functions. This is the first study to report the inhibitory effect of melatonin on osteoclastic activation by microgravity. We also observed a novel action pathway of melatonin on osteoclasts via an increase in CALCITONIN secretion. Melatonin could be the source of a potential novel drug to prevent bone loss during space flight.

Abstract:  Several reports indicate that melatonin is involved in the regulation of bone metabolism. To examine the direct effect of melatonin on osteoclasts and osteoblasts, we developed an in vitro assay using fish scales that contain osteoclasts, osteoblasts, and bone matrix, all of which are similar to those found in mammalian membrane bone. Using the assay, we demonstrated that melatonin suppressed osteoclastic and osteoblastic activities. These findings are in agreement with the reports from in vivo studies in mice and rats. In an attempt to develop molecules that increase bone mass, novel bromomelatonin derivatives were synthesized, and the effects of these chemicals on osteoclasts and osteoblasts using the scale assay were examined. As a result, novel bromomelatonin derivatives with the ability to possibly increase bone formation were identified. In scale osteoclasts, particularly, 1‐benzyl‐2,4,6‐tribromomelatonin had a more potent activity than melatonin. In reference to osteoblasts, this agent (10⁻⁹–10⁻⁶m) significantly activated osteoblasts. The effect of 1‐benzyl‐2,4,6‐tribromomelatonin on bone formation was confirmed in ovariectomized rats. Thus, the oral administration of 1‐benzyl‐2,4,6‐tribromomelatonin augmented the total bone mineral density of the femoral metaphysis of ovariectomized rats. The stress–strain index of the diaphysis in 1‐benzyl‐2,4,6‐tribromomelatonin‐treated rats significantly increased in comparison with that in ovariectomized rats. In rats fed a low‐calcium diet, the total bone mineral density of the femoral metaphysis significantly increased following the oral administration of 1‐benzyl‐2,4,6‐tribromomelatonin. These studies identified a melatonin derivative that may have potential use in the treatment of bone diseases, such as osteoporosis.