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Ferrocenyl (Fc) conjugates (1–3) of alkylpyridinium cations (E)‐N‐alkyl‐4‐[2‐(ferrocenyl)vinyl]pyridinium bromide (alkyl = n‐butyl in 1, N,N,N‐triethylbutan‐1‐aminium bromide in 2, and n‐butyltriphenylphosphonium bromide in 3) were prepared and characterized, and their photocytotoxicities and cellular uptakes in HeLa cancer and 3T3 normal cells were studied. The species with a 4‐methoxyphenyl moiety (4) instead of Fc was used as a control. The triphenylphosphonium‐appended 3 was designed for specific delivery into the mitochondria of the cells. Compounds 1–3 showed metal‐to‐ligand charge‐transfer bands at λ ≈ 550 nm in phosphate buffered saline (PBS). The Fc+/Fc and pyridinium core redox couples were observed at 0.75 and –1.2 V versus a saturated calomel electrode (SCE) in CH2Cl2/0.1 M (nBu4N)ClO4. Conjugate 3 showed a significantly higher photocytotoxicity in HeLa cancer cells [IC50 = (1.3 ± 0.2) μM] than in normal 3T3 cells [IC50 = (27.5 ± 1.5) μM] in visible light (400–700 nm). The positive role of the Fc moiety in 3 was evident from the inactive nature of 4. A JC‐1 dye (5,5,6,6‐tetrachloro‐1,1,3,3‐tetraethylbenzimidazolylcarbocyanine iodide) assay showed that 3 targets the mitochondria and induces apoptosis by the mitochondrial intrinsic pathway caused by reactive oxygen species (ROS). Annexin/propidium iodide studies showed that 3 induces apoptotic cell death in visible light by ROS generation, as evidenced from dichlorofluorescein diacetate assay. Compounds 1–3 exhibit DNA photocleavage activity through the formation of hydroxyl radicals.

Marine molluscs are widely distributed throughout the world and many bioactive compounds exhibiting antiviral, antitumor, antileukemic, and antibacterial activity have been reported worldwide. The present study was designed to investigate the beneficial effect of methanol extract of Euchelus asper (EAME) on estrogen deficiency induced osteoporosis in ovariectomised mice model. Forty-two female Swiss albino mice were randomly assigned into Sham operated (Sham) group and six ovariectomised (OVX) subgroups such as OVX with vehicle (OVX); OVX with estradiol (2 mg/kg/day); OVX with EAME of graded doses (25, 50, 100, and 200 mg/kg/day). Bone turnover markers like serum alkaline phosphatase (ALP), serum acid phosphatase (ACP), serum calcium, and histological investigations of tibia and uterus were analysed. Metaphyseal DNA content of the femur bone was also studied. Antiosteoclastogenic activity of EAME was examined. Administration of EAME was able to reduce the increased bone turnover markers in the ovariectomised mice. Histomorphometric analysis revealed an increase in bone trabeculation and restoration of trabecular separation by EAME treatment. Metaphyseal DNA content of the femur of the OVX mice was increased by EAME administration. EAME also showed a potent antiosteoclastogenic behaviour. Thus, the present study reveals that EAME was able to successfully reduce the estrogen deficiency induced bone loss.

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