Gert Maritz - Academia.edu (original) (raw)
Papers by Gert Maritz
Reproduction, Fertility and Development, 1998
The aim of this study was to investigate the effect of maternal nicotine exposure during pregnanc... more The aim of this study was to investigate the effect of maternal nicotine exposure during pregnancy and lactation on the development of the lungs of the offspring as a gas- exchanger. Pregnant rats received nicotine (1 mg/kg body mass day–1) subcutaneously during gestation and lactation. Nicotine administration started one day after mating and lasted until weaning on post natal Day 21. The offspring were exposed to nicotine only via the placenta and the milk of the mother. The lung tissue of the neonates was collected on post natal Days 14, 21, 35 and 42 and prepared for morphometry. The results obtained show that maternal nicotine exposure suppressed alveolarisation in the lungs of the offspring, which resulted in a reduced internal surface area available for gas exchange. The radial alveolar count as well as the number of capillaries in the septa were also significantly lower than in the control animals. It is concluded that maternal nicotine exposure had an adverse effect on the development of the gas exchange region of the lungs of the offspring that persisted at least up to Day 42 after birth.
Cell Biology International, Jun 1, 1993
There have been a few studies that examined the oxidative stress effects of nicotine during pregn... more There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. We aimed to determine the adverse effects of maternal nicotine exposure during pregnancy and lactation on oxidant-antioxidant system, and to determine a protective effect of ascorbic acid (Asc). Gravid rats were assigned into four groups. In Group 1, pregnant rats received 6-mg/kg/day nicotine subcutaneously during pregnancy from 1 to 21 days of gestation and lactation (until postnatal day 21). Group 2 received nicotine and Asc for the same period. In Group 3, the rats received nicotine during lactation. Control pregnant rats (Group 4) received only saline subcutaneously. Serum malondialdehyde (MDA), myeloperoxidase (MPO), and superoxide dismutase (SOD) levels were determined at 21 days of age. Nicotine exposure decreased birth weight and pregnancy weight gain. MDA values of the rat pups exposed to nicotine in both Groups 1 and 2 were higher than those of control and Group 3. SOD and MPO values of the groups were similar. Mean birth weight and serum MDA levels of Groups 1 and 2 were similar. Nicotine exposure via placental transfer increases oxidative stress as manifested by an increase in MDA level. Asc supplementation does not prevent the adverse effects of maternal nicotine exposure.
Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology, Jun 1, 1997
There have been a few studies that examined the oxidative stress effects of nicotine during pregn... more There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. We aimed to determine the adverse effects of maternal nicotine exposure during pregnancy and lactation on oxidant-antioxidant system, and to determine a protective effect of ascorbic acid (Asc). Gravid rats were assigned into four groups. In Group 1, pregnant rats received 6-mg/kg/day nicotine subcutaneously during pregnancy from 1 to 21 days of gestation and lactation (until postnatal day 21). Group 2 received nicotine and Asc for the same period. In Group 3, the rats received nicotine during lactation. Control pregnant rats (Group 4) received only saline subcutaneously. Serum malondialdehyde (MDA), myeloperoxidase (MPO), and superoxide dismutase (SOD) levels were determined at 21 days of age. Nicotine exposure decreased birth weight and pregnancy weight gain. MDA values of the rat pups exposed to nicotine in both Groups 1 and 2 were higher than those of control and Group 3. SOD and MPO values of the groups were similar. Mean birth weight and serum MDA levels of Groups 1 and 2 were similar. Nicotine exposure via placental transfer increases oxidative stress as manifested by an increase in MDA level. Asc supplementation does not prevent the adverse effects of maternal nicotine exposure.
Cell Biology International Reports, 1992
The aim of the present study was to establish whether ascorbic acid supplementation (1 mg/kg/body... more The aim of the present study was to establish whether ascorbic acid supplementation (1 mg/kg/body mass/day) during pregnancy and lactation will prevent the effect of maternal nicotine exposure (1 mg/kg/body weight/day) on neonatal lung carbohydrate, DNA and protein metabolism. The data show that the adult lung ascorbic acid content was reduced by 76% after exposure to nicotine. In contrast, maternal nicotine exposure during pregnancy and lactation has no effect on neonatal lung ascorbic acid content. However, ascorbic acid supplementation during pregnancy and lactation prevented the adverse effects of maternal nicotine exposure on neonatal lung carbohydrate, DNA and protein metabolism.
Pathophysiology, Apr 1, 1995
The influence of maternal nicotine exposure (1 mg/kg body mass/day, SC) on the biochemical respon... more The influence of maternal nicotine exposure (1 mg/kg body mass/day, SC) on the biochemical response of neonatal lung was investigated. Maternal nicotine exposure during pregnancy suppressed glycolysis irreversibly and thus energy supply to especially type I epithelial cells. The lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and glucose 6-phosphate dehydrogenase (G6PDH) activity in bronchoalveolar lavage (BAL) increased, thereby indicating damage to type I and II cells. The lower total lung G6PDH activity of the neonatal lungs exposed to nicotine might reduce the capacity of the lung to protect itself against foreign substances to which it is exposed, thereby rendering it more susceptible to damage.
Cell Biology International, Jul 1, 1994
Clinical and Experimental Pharmacology and Physiology, Mar 4, 2000
Intrauterine growth restriction (IUGR) affects vascular reactivity in older rats, but at present ... more Intrauterine growth restriction (IUGR) affects vascular reactivity in older rats, but at present the causative factors for this change are unknown. Therefore, we investigated downstream events associated with vascular reactivity, specifically, Ca 2+-regulated force production and shifts in contractile protein content. The mesenteric artery from male and female 1-year-old Wistar-Kyoto rats was examined using two distinct experimental growth restriction models. Uterine ligation surgery restriction or a sham surgery was conducted at day 18 of pregnancy, whilst a food restriction diet (40% control diet) began on gestational day 15. Extracellular vascular reactivity was studied using intact mesenteric arteries, which were subsequently chemically permeabilized using 50 μM β-escin to examine Ca 2+-activated force. Peak contractile responses to a K +-induced depolarization and phenylephrine were significantly elevated due to an increase in maximum Ca 2+-activated force in the male surgery restricted group. No changes in contractile forces were reported between female experimental groups. Sections of mesenteric artery were examined using western blotting, revealing IUGR increased the relative abundance of the voltage-gated Ca 2+ channel, inositol-1,4,5-trisphosphate receptor and myosin light chain kinase, in both male growth restricted groups, whereas no changes were seen in females. These findings demonstrate for the first time in 1-year-old rats that changes in vascular reactivity due to IUGR are caused by a change in Ca 2+-activated force and shifts in important contractile protein content. These changes affect the Wistar-Kyoto rat in a sex-specific and maternal insult-dependent manner. Keywords Ca 2+-activated force. Contractile proteins. Intrauterine growth restriction. Resistance arteries. Vascular smooth muscle Key points • IUGR increased maximum Ca 2+-activated force in male resistance arteries • Concurrent increase in contractile protein expression of male IUGR arteries • No contractile or biochemical changes in female IUGR mesenteric arteries • Sex-specific and maternal insult-dependent effect of IUGR on resistance arteries Electronic supplementary material The online version of this article (
American Journal of Physiology-lung Cellular and Molecular Physiology, Mar 1, 2009
Journal of Health Psychology, Mar 1, 2007
The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the f... more The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the fact that nicotine impairs, disrupts, duplicates and/or interacts with essential physiological functions and is involved in tobacco-related carcinogenesis. The main concerns in the present context are its fetotoxicity and neuroteratogenicity that can cause cognitive, affective and behavioral disorders in children born to mothers exposed to nicotine during pregnancy, and the detrimental effects of nicotine on the growing organism. Hence, the use of nicotine, whose efficacy in treating nicotine addiction is controversial even in adults, must be strictly avoided in pregnancy, breastfeeding, childhood and adolescence.
American Thoracic Society International Conference, 1999
Physiology News, 2005
Short news items are encouraged and can usually be included as late copy if space permits. Sugges... more Short news items are encouraged and can usually be included as late copy if space permits. Suggestions for articles Suggestions for future articles are welcome. Please contact either the Editorial Administrator or a member of the Editorial Group of Physiology News (see contents page for details).
... 2001). At 8 weeks, the thicknesses of components of airway walls were not different between g... more ... 2001). At 8 weeks, the thicknesses of components of airway walls were not different between groups; however, we observed that submucosal gland profiles were less numerous in IUGR lambs, whereas epithelial mucin content was increased (Wignarajah et al. 2002). ...
The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the f... more The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the fact that nicotine impairs, disrupts, duplicates and/or interacts with essential physiological functions and is involved in tobacco-related carcinogenesis. The main concerns in the present context are its fetotoxicity and neuroteratogenicity that can cause cognitive, affective and behavioral disorders in children born to mothers exposed to nicotine during pregnancy, and the detrimental effects of nicotine on the growing organism. Hence, the use of nicotine, whose efficacy in treating nicotine addiction is controversial even in adults, must be strictly avoided in pregnancy, breastfeeding, childhood and adolescence. Journal of Health Psychology Copyright © 2007 SAGE Publications London, Thousand Oaks and New Delhi, www.sagepublications.com Vol 12(2) 215–224 DOI: 10.1177/1359105307074240
Experimental Lung Research, 2003
The ailll of this investigation was to determine whether nicotine exposure (1 lllglkg body lllass... more The ailll of this investigation was to determine whether nicotine exposure (1 lllglkg body lllass/d) during pregnancy and lactation contributes to the rupturing of alveolar septa in the lungs of neonatal rats. These rats received nicotine only via the placenta and lllother's ntilk. The results show that tnaternal nicotine exposure interferes with elastic tissue fOrlllation. It also interferes with alveoli fOrlllation and causes the developlllent of elllphysellla-like lesions. It is therefore suggested that lllaternal nicotine intake frolll sllloking during pregnancy and lactation lllay interfere with lung developlllent and lllaturation to an extent that increases susceptibility to elllphysema.
South African Journal of Botany, 2017
Edited by D De Beer Antimutagenesis studies against the tobacco-specific mutagens 4-(methylnitros... more Edited by D De Beer Antimutagenesis studies against the tobacco-specific mutagens 4-(methylnitrosamino)-1-(3-pyridyl)-1butanone (NNK) and N-oxide, 4 (methyl-nitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), were conducted using hot water aqueous extracts of rooibos (Aspalathus linearis), honeybush (Cyclopia intermedia), and cancer bush (Sutherlandia frutescens). Aqueous extracts of both "fermented" and "unfermented" (green) rooibos and honeybush were included, while extracts of green and black teas (Camellia sinensis) served as benchmarks. A polyphenol-enriched methanol extract of unfermented rooibos (RgM) was included to further elucidate the possible role of rooibos polyphenols. Studies were performed in the presence of the metabolic activation against Salmonella typhimurium tester strain TA1535, using the standard plate incorporation and micro-suspension, preincubation assays. The mutagenic effects of NNK against the strain TA1535 was best demonstrated using the standard plate incorporation assay, while a higher mutagenicity was demonstrated for NNAL using the microsuspension, pre-incubation method. Black tea and RgM exhibited the highest protection against NNK-induced mutagenesis followed by the aqueous extracts of rooibos ≥ green tea ≥ honeybush ≥ cancer bush. Black tea, green tea, RgM and unfermented rooibos were the most effective against NNAL-induced mutagenesis, followed by fermented rooibos. The two honeybush extracts exhibited similar, but the weakest protective response. When considering the amount of total polyphenols (TPP) incorporated in the plate incorporation assay, cancer bush exhibited similar protection to that of fermented and unfermented honeybush against NNK mutagenesis. The involvement of specific polyphenol-cytochrome P450 (CYP450) interactions is likely to be involved in the protection against tobacco-related mutagenesis. Polyphenol constituents of rooibos, honeybush and cancer bush could play an important role in the protection against mutagenesis induced by the major tobacco-specific carcinogens.
Physiology News, Apr 1, 2005
Short news items are encouraged and can usually be included as late copy if space permits. Sugges... more Short news items are encouraged and can usually be included as late copy if space permits. Suggestions for articles Suggestions for future articles are welcome. Please contact either the Editorial Administrator or a member of the Editorial Group of Physiology News (see contents page for details).
Reproduction, Fertility and Development, 1998
The aim of this study was to investigate the effect of maternal nicotine exposure during pregnanc... more The aim of this study was to investigate the effect of maternal nicotine exposure during pregnancy and lactation on the development of the lungs of the offspring as a gas- exchanger. Pregnant rats received nicotine (1 mg/kg body mass day–1) subcutaneously during gestation and lactation. Nicotine administration started one day after mating and lasted until weaning on post natal Day 21. The offspring were exposed to nicotine only via the placenta and the milk of the mother. The lung tissue of the neonates was collected on post natal Days 14, 21, 35 and 42 and prepared for morphometry. The results obtained show that maternal nicotine exposure suppressed alveolarisation in the lungs of the offspring, which resulted in a reduced internal surface area available for gas exchange. The radial alveolar count as well as the number of capillaries in the septa were also significantly lower than in the control animals. It is concluded that maternal nicotine exposure had an adverse effect on the development of the gas exchange region of the lungs of the offspring that persisted at least up to Day 42 after birth.
Cell Biology International, Jun 1, 1993
There have been a few studies that examined the oxidative stress effects of nicotine during pregn... more There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. We aimed to determine the adverse effects of maternal nicotine exposure during pregnancy and lactation on oxidant-antioxidant system, and to determine a protective effect of ascorbic acid (Asc). Gravid rats were assigned into four groups. In Group 1, pregnant rats received 6-mg/kg/day nicotine subcutaneously during pregnancy from 1 to 21 days of gestation and lactation (until postnatal day 21). Group 2 received nicotine and Asc for the same period. In Group 3, the rats received nicotine during lactation. Control pregnant rats (Group 4) received only saline subcutaneously. Serum malondialdehyde (MDA), myeloperoxidase (MPO), and superoxide dismutase (SOD) levels were determined at 21 days of age. Nicotine exposure decreased birth weight and pregnancy weight gain. MDA values of the rat pups exposed to nicotine in both Groups 1 and 2 were higher than those of control and Group 3. SOD and MPO values of the groups were similar. Mean birth weight and serum MDA levels of Groups 1 and 2 were similar. Nicotine exposure via placental transfer increases oxidative stress as manifested by an increase in MDA level. Asc supplementation does not prevent the adverse effects of maternal nicotine exposure.
Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology, Jun 1, 1997
There have been a few studies that examined the oxidative stress effects of nicotine during pregn... more There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. We aimed to determine the adverse effects of maternal nicotine exposure during pregnancy and lactation on oxidant-antioxidant system, and to determine a protective effect of ascorbic acid (Asc). Gravid rats were assigned into four groups. In Group 1, pregnant rats received 6-mg/kg/day nicotine subcutaneously during pregnancy from 1 to 21 days of gestation and lactation (until postnatal day 21). Group 2 received nicotine and Asc for the same period. In Group 3, the rats received nicotine during lactation. Control pregnant rats (Group 4) received only saline subcutaneously. Serum malondialdehyde (MDA), myeloperoxidase (MPO), and superoxide dismutase (SOD) levels were determined at 21 days of age. Nicotine exposure decreased birth weight and pregnancy weight gain. MDA values of the rat pups exposed to nicotine in both Groups 1 and 2 were higher than those of control and Group 3. SOD and MPO values of the groups were similar. Mean birth weight and serum MDA levels of Groups 1 and 2 were similar. Nicotine exposure via placental transfer increases oxidative stress as manifested by an increase in MDA level. Asc supplementation does not prevent the adverse effects of maternal nicotine exposure.
Cell Biology International Reports, 1992
The aim of the present study was to establish whether ascorbic acid supplementation (1 mg/kg/body... more The aim of the present study was to establish whether ascorbic acid supplementation (1 mg/kg/body mass/day) during pregnancy and lactation will prevent the effect of maternal nicotine exposure (1 mg/kg/body weight/day) on neonatal lung carbohydrate, DNA and protein metabolism. The data show that the adult lung ascorbic acid content was reduced by 76% after exposure to nicotine. In contrast, maternal nicotine exposure during pregnancy and lactation has no effect on neonatal lung ascorbic acid content. However, ascorbic acid supplementation during pregnancy and lactation prevented the adverse effects of maternal nicotine exposure on neonatal lung carbohydrate, DNA and protein metabolism.
Pathophysiology, Apr 1, 1995
The influence of maternal nicotine exposure (1 mg/kg body mass/day, SC) on the biochemical respon... more The influence of maternal nicotine exposure (1 mg/kg body mass/day, SC) on the biochemical response of neonatal lung was investigated. Maternal nicotine exposure during pregnancy suppressed glycolysis irreversibly and thus energy supply to especially type I epithelial cells. The lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and glucose 6-phosphate dehydrogenase (G6PDH) activity in bronchoalveolar lavage (BAL) increased, thereby indicating damage to type I and II cells. The lower total lung G6PDH activity of the neonatal lungs exposed to nicotine might reduce the capacity of the lung to protect itself against foreign substances to which it is exposed, thereby rendering it more susceptible to damage.
Cell Biology International, Jul 1, 1994
Clinical and Experimental Pharmacology and Physiology, Mar 4, 2000
Intrauterine growth restriction (IUGR) affects vascular reactivity in older rats, but at present ... more Intrauterine growth restriction (IUGR) affects vascular reactivity in older rats, but at present the causative factors for this change are unknown. Therefore, we investigated downstream events associated with vascular reactivity, specifically, Ca 2+-regulated force production and shifts in contractile protein content. The mesenteric artery from male and female 1-year-old Wistar-Kyoto rats was examined using two distinct experimental growth restriction models. Uterine ligation surgery restriction or a sham surgery was conducted at day 18 of pregnancy, whilst a food restriction diet (40% control diet) began on gestational day 15. Extracellular vascular reactivity was studied using intact mesenteric arteries, which were subsequently chemically permeabilized using 50 μM β-escin to examine Ca 2+-activated force. Peak contractile responses to a K +-induced depolarization and phenylephrine were significantly elevated due to an increase in maximum Ca 2+-activated force in the male surgery restricted group. No changes in contractile forces were reported between female experimental groups. Sections of mesenteric artery were examined using western blotting, revealing IUGR increased the relative abundance of the voltage-gated Ca 2+ channel, inositol-1,4,5-trisphosphate receptor and myosin light chain kinase, in both male growth restricted groups, whereas no changes were seen in females. These findings demonstrate for the first time in 1-year-old rats that changes in vascular reactivity due to IUGR are caused by a change in Ca 2+-activated force and shifts in important contractile protein content. These changes affect the Wistar-Kyoto rat in a sex-specific and maternal insult-dependent manner. Keywords Ca 2+-activated force. Contractile proteins. Intrauterine growth restriction. Resistance arteries. Vascular smooth muscle Key points • IUGR increased maximum Ca 2+-activated force in male resistance arteries • Concurrent increase in contractile protein expression of male IUGR arteries • No contractile or biochemical changes in female IUGR mesenteric arteries • Sex-specific and maternal insult-dependent effect of IUGR on resistance arteries Electronic supplementary material The online version of this article (
American Journal of Physiology-lung Cellular and Molecular Physiology, Mar 1, 2009
Journal of Health Psychology, Mar 1, 2007
The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the f... more The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the fact that nicotine impairs, disrupts, duplicates and/or interacts with essential physiological functions and is involved in tobacco-related carcinogenesis. The main concerns in the present context are its fetotoxicity and neuroteratogenicity that can cause cognitive, affective and behavioral disorders in children born to mothers exposed to nicotine during pregnancy, and the detrimental effects of nicotine on the growing organism. Hence, the use of nicotine, whose efficacy in treating nicotine addiction is controversial even in adults, must be strictly avoided in pregnancy, breastfeeding, childhood and adolescence.
American Thoracic Society International Conference, 1999
Physiology News, 2005
Short news items are encouraged and can usually be included as late copy if space permits. Sugges... more Short news items are encouraged and can usually be included as late copy if space permits. Suggestions for articles Suggestions for future articles are welcome. Please contact either the Editorial Administrator or a member of the Editorial Group of Physiology News (see contents page for details).
... 2001). At 8 weeks, the thicknesses of components of airway walls were not different between g... more ... 2001). At 8 weeks, the thicknesses of components of airway walls were not different between groups; however, we observed that submucosal gland profiles were less numerous in IUGR lambs, whereas epithelial mucin content was increased (Wignarajah et al. 2002). ...
The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the f... more The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the fact that nicotine impairs, disrupts, duplicates and/or interacts with essential physiological functions and is involved in tobacco-related carcinogenesis. The main concerns in the present context are its fetotoxicity and neuroteratogenicity that can cause cognitive, affective and behavioral disorders in children born to mothers exposed to nicotine during pregnancy, and the detrimental effects of nicotine on the growing organism. Hence, the use of nicotine, whose efficacy in treating nicotine addiction is controversial even in adults, must be strictly avoided in pregnancy, breastfeeding, childhood and adolescence. Journal of Health Psychology Copyright © 2007 SAGE Publications London, Thousand Oaks and New Delhi, www.sagepublications.com Vol 12(2) 215–224 DOI: 10.1177/1359105307074240
Experimental Lung Research, 2003
The ailll of this investigation was to determine whether nicotine exposure (1 lllglkg body lllass... more The ailll of this investigation was to determine whether nicotine exposure (1 lllglkg body lllass/d) during pregnancy and lactation contributes to the rupturing of alveolar septa in the lungs of neonatal rats. These rats received nicotine only via the placenta and lllother's ntilk. The results show that tnaternal nicotine exposure interferes with elastic tissue fOrlllation. It also interferes with alveoli fOrlllation and causes the developlllent of elllphysellla-like lesions. It is therefore suggested that lllaternal nicotine intake frolll sllloking during pregnancy and lactation lllay interfere with lung developlllent and lllaturation to an extent that increases susceptibility to elllphysema.
South African Journal of Botany, 2017
Edited by D De Beer Antimutagenesis studies against the tobacco-specific mutagens 4-(methylnitros... more Edited by D De Beer Antimutagenesis studies against the tobacco-specific mutagens 4-(methylnitrosamino)-1-(3-pyridyl)-1butanone (NNK) and N-oxide, 4 (methyl-nitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), were conducted using hot water aqueous extracts of rooibos (Aspalathus linearis), honeybush (Cyclopia intermedia), and cancer bush (Sutherlandia frutescens). Aqueous extracts of both "fermented" and "unfermented" (green) rooibos and honeybush were included, while extracts of green and black teas (Camellia sinensis) served as benchmarks. A polyphenol-enriched methanol extract of unfermented rooibos (RgM) was included to further elucidate the possible role of rooibos polyphenols. Studies were performed in the presence of the metabolic activation against Salmonella typhimurium tester strain TA1535, using the standard plate incorporation and micro-suspension, preincubation assays. The mutagenic effects of NNK against the strain TA1535 was best demonstrated using the standard plate incorporation assay, while a higher mutagenicity was demonstrated for NNAL using the microsuspension, pre-incubation method. Black tea and RgM exhibited the highest protection against NNK-induced mutagenesis followed by the aqueous extracts of rooibos ≥ green tea ≥ honeybush ≥ cancer bush. Black tea, green tea, RgM and unfermented rooibos were the most effective against NNAL-induced mutagenesis, followed by fermented rooibos. The two honeybush extracts exhibited similar, but the weakest protective response. When considering the amount of total polyphenols (TPP) incorporated in the plate incorporation assay, cancer bush exhibited similar protection to that of fermented and unfermented honeybush against NNK mutagenesis. The involvement of specific polyphenol-cytochrome P450 (CYP450) interactions is likely to be involved in the protection against tobacco-related mutagenesis. Polyphenol constituents of rooibos, honeybush and cancer bush could play an important role in the protection against mutagenesis induced by the major tobacco-specific carcinogens.
Physiology News, Apr 1, 2005
Short news items are encouraged and can usually be included as late copy if space permits. Sugges... more Short news items are encouraged and can usually be included as late copy if space permits. Suggestions for articles Suggestions for future articles are welcome. Please contact either the Editorial Administrator or a member of the Editorial Group of Physiology News (see contents page for details).