Review
DDE-induced eggshell thinning in birds: Effects of p,p′-DDE on the calcium and prostaglandin metabolism of the eggshell gland

https://doi.org/10.1016/S0742-8413(97)00105-9Get rights and content

Abstract

  • 1.

    1. The focus of this review is the effects and mechanism of action of p,p′-DDE on eggshell formation in birds. Inhibition of prostaglandin synthesis in the eggshell gland mucosa is a probable mechanism for p,p′-DDE-induced eggshell thinning.

  • 2.

    2. The duck is sensitive to p,p′-DDE-induced eggshell thinning but the domestic fowl is not, and studies comparing the two species in regard to the calcium and prostaglandin metabolism of the eggshell gland have shown that eggshell thinning induced by p,p′-DDE in ducks is accompanied by reduced activity of prostaglandin synthetase, reduced levels of prostaglandin E2, and reduced uptake of 45Ca by the eggshell gland mucosa. The content of calcium, bicarbonate, chloride, sodium, and potassium are also reduced in the eggshell gland lumen in ducks exhibiting eggshell thinning. None of these effects are seen in the domestic fowl.

  • 3.

    3. Inhibition of prostaglandin synthesis is a specific effect of p,p′-DDE. The detrimental effects of p,p′-DDE on the eggshell gland seem to be unique when comparing the compound with structurally related substances, i.e., similar treatment regimens with o,p′-DDE, p,p′-DDT, o,p′-DDT, and p,p′-DDD do not cause eggshell thinning in ducks. Neither do they inhibit prostaglandin synthesis in the eggshell gland mucosa.

  • 4.

    4. Administration of other compounds that do inhibit prostaglandin synthesis, e.g., indomethacin, does cause the same effects as those seen with p,p′-DDE, i.e., eggshell thinning and the described effects on the calcium and prostaglandin metabolism of the eggshell gland.

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      However, the third and leading hypothesis to the main causes of chemically-induced eggshell thinning by DDE was the inhibition of the excretion of calcium, and to a lesser degree carbonate, from the shell gland to the uterine cavity (Cooke, 1973; Lundholm, 1997; Holm et al., 2006). Subsequent studies attempting to elucidate the mechanism of action of DDE demonstrated that decreased calcium excretion was largely mediated through the inhibition of the synthesis of cyclooxygenases, and subsequently prostaglandins (Lundholm, 1997). Cyclooxygenases are enzymes responsible for forming prostanoid eicosanoids, a diverse array of lipid-based signaling molecules, including prostaglandins, thromboxanes, and prostacyclins (Alexanian and Sorokin, 2017).

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