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Hexachlorobenzene (HCB) is a pesticide that is constantly produced as a by-product in many industrial processes. Rutin (RUT) is a flavonoid found in many plants with numerous biological and pharmacological properties. However, there is no scientifical information on the impact of RUT on HCB-induced reproductive toxicity in male rats. Thus, we investigated the effect of rutin on HCB-induced reproductive toxicity. Rats were divided into four groups consisting of control administered with corn oil, HCB alone (16 mg/kg), RUT alone (100 mg/kg) and HCB + RUT that were treated orally by gavage for 28 days. Hexachlorobenzene caused a significant reduction in epididymal sperm count, sperm progressive motility, viability, number of hypo-osmotic tail swelled spermatozoa and increased sperm morphological abnormalities (head, midpiece and tail). Furthermore, HCB decreased the activities of gamma glutamyl transferase, lactate dehydrogenase, sorbitol dehydrogenase, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, levels of glutathione and total protein with increased malondialdehyde level. Additionally, HCB increased the levels of total cholesterol, low density lipoprotein, triglycerides, follicle stimulating hormone, luteinizing hormone but decreased high density lipoproteins, serum testosterone, steroidogenic enzymes (3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase), B-cell lymphoma and increased pro-apoptotic markers (Bcl-2 associated protein (Bax), caspases-3 and-9) alongside histological and histomorphometrical abnormalities. Nevertheless, RUT prevented all the aberrations caused by HCB. Our result showed that HCB induced reproductive toxicity in rats and RUT protected against HCB-induced r reproductive toxicity.

Atrazine (ATZ) is an environmental pollutant that interferes with several aspects of mammalian cellular processes including germ cell development, immunological, reproductive and neurological functions. At the level of human exposure, ATZ reduces sperm count and contribute to infertility in men. ATZ also induces morphological changes similar to apoptosis and initiates mitochondria-dependent cell death in several experimental models. When in vitro experimental models are exposed to ATZ, they are faced with increased levels of reactive oxygen species (ROS), cytotoxicity and decreased growth rate at dosages that may vary with cell types. This results in differing cytotoxic responses that are influenced by the nature of target cells, assay types and concentrations of ATZ. However, oxidative stress could play salient role in the observed cellular and genetic toxicity and apoptosis-like effects which could be abrogated by antioxidant vitamins and flavonoids, including vitamin E, quercetin, kolaviron, myricetin and bioactive extractives with antioxidant effects. This review focuses on the differential responses of cell types to ATZ toxicity, testicular effects of ATZ in both in vitro and in vivo models and chemopreventive strategies, so as to highlight the current state of the art on the toxicological outcomes of ATZ exposure in several experimental model systems.

Ulcerative colitis is an idiopathic disease attributed to an aggressive dysregulated immune response that results in epithelial injury and diffuse inflammation in the colon. Ulcerative colitis may be acute or chronic with unpredictable relapse. Kolaviron, a bioflavonoid extracted from Garcinia kola has been reported to possess gastroprotective properties. We have previously reported the protective effect of kolaviron on acute colitis. This study investigated the effect of kolaviron on dextran sulphate sodium-induced chronic ulcerative colitis in Balb/c mice. Mice were randomly assigned to four groups of 10 mice each. Group I (Control) mice received corn oil at 2 ​ml/kg for forty-nine days. Group II mice received kolaviron at 200 ​mg/kg for forty-nine days. Group III mice received 3 cycles of dextran sulphate sodium (DSS) (2.5% w/v) in drinking water (each cycle is defined as 7 days of 2.5% DSS followed by 7 days of normal drinking water). Group IV received Kolaviron at 200 ​mg/kg body weight for 7 days before co-administration with 3 cycles of DSS (2.5% w/v). Administration of kolaviron significantly ameliorated increases in disease activity index in DSS-induced chronic ulcerative colitis in mice. Furthermore, kolaviron suppresses the expression of inducible nitric oxide synthase and cyclooxygenase-2 in DSS-treated mice. Additionally, kolaviron protected against colonic oxidant stress damage by augmenting the endogenous antioxidant with concomitant decrease in myeloperoxidase activity, tumor necrosis factor alpha, Interleukin-1β, and lipid peroxidation levels in DSS-treated mice. Moreover, kolaviron attenuated the disruption of the colonic histological architecture and reduced neutrophil infiltration in DSS-treated mice. In conclusion, kolaviron ameliorated DSS-induced chronic ulcerative colitis via antioxidant and anti-inflammatory mechanisms.

Perfluorooctanoic acid (PFOA) is a contaminant of global concern owing to its prevalent occurrence in aquatic and terrestrial environments with potential hazardous impact on living organisms. Here, we investigated the influence of realistic environmental concentrations of PFOA (0, 0.25, 0.5, or 1.0 mg/L) on relevant behaviors of adult zebrafish (Danio rerio) (e.g., exploration to novelty, social preference, and aggression) and the possible role of PFOA in modulating cholinergic and purinergic signaling in the brain after exposure for 7 consecutive days. PFOA significantly increased geotaxis as well as reduced vertical exploration (a behavioral endpoint for anxiety), and increased the frequency and duration of aggressive episodes without affecting their social preference. Exposure to PFOA did not affect ADP hydrolysis, whereas ATP and AMP hydrolysis were significantly increased at the highest concentration tested. However, AChE activity was markedly decreased in all PFOA-exposed groups when compared with control. In conclusion, PFOA induces aggression and anxiety-like behavior in adult zebrafish and modulates both cholinergic and purinergic signaling biomarkers. These novel data can provide valuable insights into possible health threats related to human activities, demonstrating the utility of adult zebrafish to elucidate how PFOA affects neurobehavioral responses in aquatic organisms.

Environmental pollution is a global concern because of its associated risks to human health and ecosystem. The bio-monitoring of environmental health has attracted much attention in recent years and efforts to minimize environmental contamination as well as to delineate toxicological mechanisms related to toxic exposure are essential to improve the health conditions of both humans and animals. This review aims to substantiate the need and advantages in utilizing cockroaches as a complementary, non-mammalian model to further understand the noxious impact of environmental contaminants on humans and animals. We discuss recent advances in neurotoxicology, immunotoxicology, reproductive and developmental toxicology, environmental forensic entomotoxicology, and environmental toxicology that corroborate the utility of the cockroach (Periplaneta americana, Blaptica dubia, Blattella germanica and Nauphoeta cinerea) in addressing toxicological mechanisms as well as a sensor of environmental pollution. Indeed, recent improvements in behavioural assessment and the detection of potential biomarkers allow for the recognition of phenotypic alterations in cockroaches following exposure to toxic chemicals namely saxitoxin, methylmercury, polychlorinated biphenyls, electromagnetic fields, pharmaceuticals, polycyclic aromatic hydrocarbon, chemical warfare agents and nanoparticles. The review provides a state-of-the-art update on the current utility of cockroach models in various aspects of toxicology as well as discusses the potential limitations and future perspectives.