“…Furthermore, lack of boron can also damage immune and reproductive functions in animals, leading to exacerbated adjuvant arthritis, testicular and ovarian atrophy, decreased sperm count, increased sperm deformity, blocked oocyte maturation in rats, and impaired mouse embryo development. , In addition, reduced plasma steroids, alkaline phosphatase, and calcium and magnesium ion concentrations have been reported to be caused by boron insufficiency. , Appropriate boron supplementation can increase the mRNA levels of bone-growth-related genes in mouse osteoblasts, such as type I collagen and osteocalcin, increase the plasma levels of total cholesterol, triglycerides, low-density lipoprotein, glucose, insulin, and non-esterified fatty acids in pregnant cows, and improve the metabolism during the perinatal phase . Furthermore, sufficient boron levels can enhance the activity of long-term cryopreserved mesenchymal stem cells and promote osteoblast and chondrocyte differentiation from human tooth germ stem cells, increase animal growth performance and feed conversion, improve egg quality, increase the level of antibodies in rats injected with human typhoid vaccine, and reduce the number of circulating natural killer (NK) cells and CD8a + /CD4 – cells. , However, supplementation with high doses of boron or high levels of boron exposure can result in significant injuries and even toxicity in animals, increase prenatal fetal mortality, reduce fetal weight and organ weight, and damage cardiovascular and central nervous systems as well as the bone development of fetuses . Moreover, supplementation with high doses of boron has been shown to induce testicular atrophy, seminiferous tubule abnormalities, and spermatogenic cell loss and block sperm development and discharge as well as cause the formation of bi- and micronucleated lymphocytes and acute leukemia cells in vitro , leading to mitochondrial swelling and an increase of the number of apoptotic cells .…”