Substances Effects
BPA= –Affect reproduction, metabolism, pubertal development, childhood growth, neurodevelopment.
-(Perinatal & neonatal exposure) organizational effects to organs
– (Pregnant rats) increase testosterone and estradiol, degreased progesterone in adulthood, and altered releasing gnRH hormone secretion. Altered ovarian with many cysts. Reduced fertility.
– Decreased basal epithelial permeability, increased response pain in the gut.
-(Prenatal ) lifelong effect on the immune defence. Predispose female offspring. Increased inflammation of the colon. Male (rats) down regulation of ERβ.
-(Pregnancy) altered mothers glucose metabolism. Suggested connection between gestational diabetes and increased risk for obesity and type II diabetes. (pregnancy on mice) increased insulin resistance, decreased glucose tolerance. Increase in plasma, insulin, leptin, triglyceride, glycerol
(Applied to humans) increased risk type II diabetes and cardiovascular disease.
-(Uterine exposure) predisposes offspring to high birth weight and obesity in adulthood. Effects on cell cycle modification can lead to to diabetic incidences later in life.
Male offsprings, had altered glucose tolerance and insulin resistance.
-(Genetically susceptible mice) Increased airway hyper responsiveness, eosinophilic inflammination, allergen-specific IgE.
– (Exposure to human fetal) reduce of testosterone and other hormones that cause the testicles to sacs.
-(Exposure to pregnant woman) may be the causes of congenital masculinisation defects.
– Possible that it decreases sperm and increases the possibility of testicular cancer.
Bis-GMA= – Irreversible effects on the cellular metabolism.
– Undesirable pulpal reaction.
– Impaired psychosocial function in children.
– No normal biological responses of pulp reaction, allergic and estrogenic effects.
– Induce a rapid and intense decline of the glutathione pool of HGFs combined with induction of apoptosis.
– Stimulate ERK phosphorylation, PGE2roduction, COX-2 mRNA, protein expression and ROS production.
– Long term effects, ability to affect the migration and tenascin expression of keratinocytes and human gingival, firoblast, disturbing the healing of injured oral tissues.
-Increase micronuclei.
BPO= – Cytotoxic to human fibroblast by inducing cell cycle arrest and cell death mainly in the form of necrosis.
CQ= -Cytotoxic submandibular duct cell line, to human gingival and pulp fibroblast.
– Cytotoxic to human fibroblast by inducing cell cycle arrest and cell death mainly in the form of necrosis.
– DNA strand breakages in cell free environment.
DEGDMA= – Pulp reactions, allergic and estrogenic effects.
DMAEMA= – Cytotoxic to human fibroblast by inducing cell cycle arrest and cell death mainly in the form of necrosis.
DMPT= – Cytotoxic to human fibroblast by inducing cell cycle arrest and cell death mainly in the form of necrosis.
EGDMA= – Pulp reactions, allergic and estrogenic effects.
– Promote the growth and proliferation of caries relevant bacteria ( S. Sobrinus L. Acidophilus) this leads to pulpal inflammation and secondary caries formation.
HEMA= – Detrimental effects to the pulpal homeostasis and repair.
– Immortalized 3T3-fibroblast cultures.
– Remarkable cytopathic effects on cultured pulp cells
-(Rats) inflammatory response through macrophages and giant cells.
– Associated with oxidative stress
– Cell death.
– Increase DNA migration whereby cell cycle delays, bur reduce in presents of antioxidants.
– Induce up-regulation of COX-2 and VEGF expressions, and suppression of Hsp72 expressions in immune cells.
Interruption of normal collagen I synthesis and the perturbation of normal differentiation processes of pulp fibroblasts into odontoblast.
TEGDMA= – Detrimental effects to the pulpal homeostasis and repair.
– Cell death
– Increase of micronuclei and promote degradation of DNA from salivary gland tissue and lymphocytes.
– DNA damage.
– Induce cytokine MCO-1 secretion from U937 cells.
Increase hydrolase in the gingival fibroblast.
– Immortalized 3T3-fibroblast cultures.
– Interaction of immune cells.
– Pulp reactions, allergic and estrogenic effects.
– (Long term exposure) effects on the immune system, wound healing, cell differentiation, cellular metabolism, differentiation processes of dental pulp fibroblast into the odontoblast and normal mineralization processes.
– DNA migration.
– Promote the growth and proliferation of caries relevant bacteria ( S. Sobrinus L. Acidophilus) this leads to pulpal inflammation and secondary caries formation.
UDMA= – Irreversible effects on the cellular metabolism.
– No normal biological responses of pulp reaction, allergic and estrogenic effects.
– Increase micronuclei.
References:
What every dentist should know about bisphenol A.
LaBauve JR, Long KN, Hack GD, Bashirelahi N.
Cytotoxicity and biocompatibility of direct and indirect pulp capping materials.
Modena KC, Casas-Apayco LC, Atta MT, Costa CA, Hebling J, Sipert CR, Navarro MF, Santos CF.
Department of Operative Dentistry, Endodontics and Dental Materials, University of São Paulo, Bauru, Brazil.
Based Dental Restorative Materials
Athina Bakopoulou,1 Triantafillos Papadopoulos,2* and Pavlos Garefis1
1Department of Fixed & Implant Prosthodontics, School of Dentistry, Aristotle University of Thessaloniki,
Thessaloniki 541 24, Greece; E-Mails:athinabakopoulou@hotmail.com (B.A.);Email: garefis@dent.auth.gr
(G.P.)
2Department of Biomaterials, School of Dentistry, National and Kapodistrian University of Athens, Athens, 115 27, Greece
-Author to whom correspondence should be addressed; EMail:trpapad@dent.uoa.gr (P.T.); Tel. +302-107-461-100; Fax: +302-107-461-306.
Differential effects of bisphenol A and diethylstilbestrol on human, rat and mouse fetal leydig cell function.
N’Tumba-Byn T, Moison D, Lacroix M, Lecureuil C, Lesage L, Prud’homme SM, Pozzi-Gaudin S, Frydman R, Benachi A, Livera G, Rouiller-Fabre V, Habert R.