In a previous study, it was shown that maternal nicotine exposure during gestation and lactation interfered with alveolarization and resulted in gradual deterioration of the lung parenchyma, resulting in microscopic emphysema. The aim of this study was thus to investigate the long-term effects of maternal nicotine exposure (1 mg/kg body weight/day, subcutaneous [sc] from the onset of the phase of rapid alveolarization, which occur from postnatal day 4 in rats, on (1) the development of the gas-exchange area of the lungs of the offspring and, (2) whether maternal copper supplementation (1 mg/kg body weight/day, SC) during the same period of time will prevent the effect of maternal nicotine exposure on the development of the neonatal rat lung. Nicotine administration lasted until weaning on postnatal day 21. The day of birth was designated day 0. The offspring were exposed to nicotine via the mother's milk only. The experimental animals received no nicotine or copper after postnatal day 21. The lung tissue of the neonates was collected on postnatal days 14, 21, and 42 and prepared for morphometry. The results obtained show that maternal nicotine exposure had no influence on body weight, chest circumference, crown-rump length, and lung volume, but resulted in bigger alveolar volumes and suppressed alveolarization in the lungs of the offspring. Copper supplementation during this period of lung development reduced the adverse effect of maternal nicotine exposure on neonatal lung development. Even though copper reduced the adverse effects of maternal nicotine exposure during this phase of lung development, it did not prevent the induction of microscopic emphysema.

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Background: Testicular insulin signalling is altered in diabetic (DM) males. While unravelling the mechanism through which DM exert these detrimental effects, studies have shown the importance of insulin regulation in glucose homeostasis, and how a lack in insulin secretion indirectly led to reduced male fertility. The current study aimed to investigate the role of rooibos, honeybush and Sutherlandia on insulin signalling in the testicular tissue of type I diabetic rats. Methods: Animals (n=60) were randomly divided into six groups. The groups include a control group, a vehicle group, and diabetes was induced in the remainder of animals via a single intraperitoneal injection of STZ at 45mg/kg. The remaining four groups included a diabetic control (DC), diabetic + rooibos (DRF), diabetic + honeybush (DHB) and diabetic + Sutherlandia group (DSL). Animals were sacrificed after seven weeks of treatment, and blood and testes were collected. Results: All diabetic groups (DC, DRF, DHB, DSL) presented with a significant increase in blood glucose levels after diabetes induction compared to the control and vehicle (p<0.001). The DC animals presented with decreased testicular protein expression of IRS-1, PkB/Akt and GLUT4 compared to controls. DRF and DHB animals displayed an acute upregulation in IRS-1, while the DSL group showed improvement in IRS-2 compared to DC. Although, DRF animals presented with a decrease in PkB/Akt, DHB and DSL animals displayed upregulation (22.3%, 48%) compared to controls, respectively. Conclusion: The results taken together, it can be suggested that these infusions may enhance insulin signalling through diverse pathways.

Rooibos (Aspalathus linearis) has various health benefits. Two case studies have associated chronic Rooibos consumption with conventional prescription medications, including atorvastatin (ATV), with hepatotoxicity. Statins act by inhibiting hydroxymethylglutaryl‐coenzyme A reductase, a rate‐limiting enzyme in cholesterol synthesis. Although rare, statins are potentially hepatotoxic. The aim was to investigate interactions between aspalathin‐rich Rooibos extract GRT™ and ATV‐induced hepatotoxicity in C3A liver cells cultured with and without palmitate. Effects of co‐treatment of GRT + ATV on cell viability, oxidative stress, apoptosis, mitochondrial integrity, and cellular reactive oxygen species (ROS) production were assessed. Significantly increased ROS production was observed in cells exposed to ATV and palmitate. Combination therapy of GRT + ATV also showed significant increases in ROS production. Under palmitate‐treated conditions, ATV‐induced significant apoptosis which was not ameliorated by GRT + ATV co‐treatment. Despite studies purporting hepatoprotection from Rooibos, our study showed that GRT was unable to modulate ATV‐induced hepatotoxic effects in this model.