Decrease, dihydrotestosterone (DHT) level ; Decrease, androgen receptors (AR) activation ; 5α-reductase, inhibition ; decrease, transcription of genes by AR ; decrease, male anogenital distance ; Altered, Transcription of genes by the androgen receptor ; Decrease, dihydrotestosterone (DHT) level ; Decrease, androgen receptor activation ; Inhibition, 5α-reductase ; decrease, transcription of genes by AR ; anogenital distance (AGD), decreased

Irreversible inhibition of hepatic VKOR by binding of AR at tyrosine 139, Failure to cycle vitamin K epoxide to vitamin K to form vitamin K hydroquinone ; Uncoupling of oxidative phosphorylation, Reduced ability to generate ATP ; Anticoagulant rodenticide interferes with carboxylation of Gla proteins in bone, Impairment of post-translational modification (carboxylation) of osteocalcin ; Under carboxylated clotting factors will not assemble on cell surfaces to form clot, Failure of secondary hemostasis ; Failure in vascular repair mechanisms, Unresolved blood loss (hemorrhage) ; Failure in gamma-glutamyl carboxylation of clotting factors II, VII, IX and X, Under carboxylation of clotting factors (e.g., des-gamma-carboxy prothrombin) ; Blood loss and development of anemia, Impaired oxygen delivery and nutrient delivery to tissue, impaired carbon dioxide and waste product removal ; Hemostasis, Depletion from blood of fully functional carboxylated clotting factors ; Reduced fitness or even mortality, Acidosis, hypovolemic shock and organ dysfunction ; Osteoporosis and vascular calcification, Bone deterioration ; Impaired recruitment , Population trajectory ; Irreversible inhibition of hepatic VKOR by binding of AR at tyrosine 139, Failure to cycle vitamin K epoxide to vitamin K to form vitamin K hydroquinone ; Uncoupling of oxidative phosphorylation, Reduced ability to generate ATP ; Anticoagulant rodenticide interferes with carboxylation of Gla proteins in bone, Impairment of post-translational modification (carboxylation) of osteocalcin ; Under carboxylated clotting factors will not assemble on cell surfaces to form clot, Failure of secondary hemostasis ; Failure in vascular repair mechanisms, Unresolved blood loss (hemorrhage) ; Failure in gamma-glutamyl carboxylation of clotting factors II, VII, IX and X, Under carboxylation of clotting factors (e.g., des-gamma-carboxy prothrombin) ; Blood loss and development of anemia, Impaired oxygen delivery and nutrient delivery to tissue, impaired carbon dioxide and waste product removal ; Hemostasis, Depletion from blood of fully functional carboxylated clotting factors ; Reduced fitness or even mortality, Acidosis, hypovolemic shock and organ dysfunction ; Osteoporosis and vascular calcification, Bone deterioration ; Impaired recruitment , Population trajectory

Inhibition, HMG-CoA reductase ; Decreased, mevalonate ; Decreased, cholesterol ; Decreased, Testosterone ; malformed, Male reproductive tract ; Decrease, Fertility ; Inhibition, HMG-CoA reductase ; Decreased, mevalonate ; Decreased, cholesterol ; Decreased, Testosterone ; malformed, Male reproductive tract ; Decrease, Fertility

Reduction, Plasma 17beta-estradiol concentrations ; Reduction, Cumulative fecundity and spawning ; Reduction, Plasma vitellogenin concentrations ; Decrease, Population trajectory ; Decrease, dihydrotestosterone (DHT) level ; 5α-reductase, inhibition ; Reduction, egg production and spawning ; Reduction, Plasma 17beta-estradiol concentrations ; Decrease, Population growth rate ; Reduction, Plasma vitellogenin concentrations ; Reduction, Cumulative fecundity and spawning ; Decrease, dihydrotestosterone (DHT) level ; Inhibition, 5α-reductase

Increase, Hyperplasia (Leydig cells) ; Increase, Leydig cell tumors ; Inhibition, 5α-reductase activity ; Increased, Leutinizing hormone (LH) ; Decrease, Bioactivation of testosterone ; Increase, Hyperplasia (Leydig cells) ; Increase, Leydig cell tumors ; Inhibition, 5α-reductase activity ; Increased, Leutinizing hormone (LH) ; Decrease, Bioactivation of testosterone

Inhibition of the enzyme 5-alpha reductase type 2 ; Decrease in dihydrotestosterone conversion from testosterone ; Decrease in transcription of androgen-dependent genes ; Alteration of proliferation and differentiation of several androgen dependent tissues ; Developmental toxicity by inhibition of the 5-alpha reductase enzyme

Inhibition of the enzyme 5-alpha reductase type 2 ; Decrease in dihydrotestosterone conversion from testosterone ; Decrease in transcription of androgen-dependent genes ; Alteration of proliferation and differentiation of several androgen dependent tissues ; Developmental toxicity by inhibition of the 5-alpha reductase enzyme ; Inhibition of the enzyme 5-alpha reductase type 2 ; Decrease in dihydrotestosterone conversion from testosterone ; Decrease in transcription of androgen-dependent genes ; Alteration of proliferation and differentiation of several androgen dependent tissues ; Developmental toxicity by inhibition of the 5-alpha reductase enzyme