Over the years, the vaste expansion of plastic manufacturing has dramatically increased the environmental impact of microplastics [MPs] and nanoplastics [NPs], making them a threat to marine and terrestrial biota because they contain endocrine disrupting chemicals [EDCs] and other harmful compounds. MPs and NPs have deleteriouse impacts on mammalian endocrine components such as hypothalamus, pituitary, thyroid, adrenal, testes, and ovaries. MPs and NPs absorb and act as a transport medium for harmful chemicals such as bisphenols, phthalates, polybrominated diphenyl ether, polychlorinated biphenyl ether, organotin, perfluorinated compounds, dioxins, polycyclic aromatic hydrocarbons, organic contaminants, and heavy metals, which are commonly used as additives in plastic production. As the EDCs are not covalently bonded to plastics, they can easily leach into milk, water, and other liquids affecting the endocrine system of mammals upon exposure. The toxicity induced by MPs and NPs is size-dependent, as smaller particles have better absorption capacity and larger surface area, releasing more EDC and toxic chemicals. Various EDCs contained or carried by MPs and NPs share structural similarities with specific hormone receptors; hence they interfere with normal hormone receptors, altering the hormonal action of the endocrine glands. This review demonstrates size-dependent MPs’ bioaccumulation, distribution, and translocation with potential hazards to the endocrine gland. We reviewed that MPs and NPs disrupt hypothalamic-pituitary axes, including the hypothalamic-pituitary-thyroid/adrenal/testicular/ovarian axis leading to oxidative stress, reproductive toxicity, neurotoxicity, cytotoxicity, developmental abnormalities, decreased sperm quality, and immunotoxicity. The direct consequences of MPs and NPs on the thyroid, testis, and ovaries are documented. Still, studies need to be carried out to identify the direct effects of MPs and NPs on the hypothalamus, pituitary, and adrenal glands.

In recent decades, the adverse effects of global warming on all living beings have been unanimously recognized across the world. A high environmental temperature that increases the respiration and rectal temperature of cattle is called heat stress (HS), and it can affect both male and female reproductive functions. For successful reproduction and fertilization, mature and healthy oocytes are crucial; however, HS reduces the developmental competence of oocytes, which compromises reproduction. HS disturbs the hormonal balance that plays a crucial role in successful reproduction, particularly in reducing the luteinizing hormone and progesterone levels, which leads to severe problems such as poor follicle development with a poor-quality oocyte and problems related to maturity, silent estrus, abnormal or weak embryo development, and pregnancy loss, resulting in a declining reproduction rate and losses for the cattle industry. Lactating cattle are particularly susceptible to HS and, hence, their reproduction rate is substantially reduced. Additionally, bulls are also affected by HS; during summer, semen quality and sperm motility decline, leading to compromised reproduction. In summer, the conception rate is reduced by 20–30% worldwide. Although various techniques, such as the provision of water sprinklers, shade, and air conditioning, are used during summer, these methods are insufficient to recover the normal reproduction rate and, therefore, special attention is needed to improve reproductive efficiency and minimize the detrimental effect of HS on cattle during summer. The application of advanced reproductive technologies such as the production of embryos in vitro, cryopreservation during the hot season, embryo transfer, and timed artificial insemination may minimize the detrimental effects of HS on livestock reproduction and recover the losses in the cattle industry.

Medicinal plants are a vital source of natural products (NPs) that can cure cancer through modulation of different pathways, including oxidative stress, extrinsic and intrinsic apoptosis, cell cycle, inflammation, NF-kB, PI3K/AKT/mTOR, AMPK (JNK), MEK/ERK (Raf)-MEK-ERK and autophagy. Puerarin (Pue), an important NP belonging to the isoflavone glycoside group, is derived from Pueraria lobata (Willd.) Ohwi, Pueraria thomsonii Benth, and Pueraria tuberosa (Willd.). This NP was approved by the Chinese Ministry of Health for the treatment of different diseases in 1993, but it was also later reported to exhibit anticancer activity. Pue causes cancer cells death through modulation of different mechanisms including oxidative stress, intrinsic and extrinsic, Survivin and XIAP, PI3K/AKT/mTOR, Ras-Raf-MEK-ERK, JNK, cell cycle, AMPK, NF-kB, inflammation and autophagy pathways. Therefore, this review compiles for the first time the studies about the anticancer mechanism of Pue and provides comprehensive information about the anticancer effects of Pue. This review may serve as a basis for future research and clinical treatment.